Sapolsky, Robert - Handouts For Human Behavioral Psychology

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012.
Hello!
This is all of my section handouts Ive made this year compiled into one document, giving a fairly detailed (though I cant
promise its comprehensive) review of class material. Its 68 pages so if youre satisfied with your current approach to
studying, pay no attention to this and carry on; dont let it distract or worry you. But for my money, IF YOU REALLY
WANT TO DO WELL ON EXAMS, this is what I recommend doing:
Look at this study guide as an example.
Create your own version of this. How?
o Gather a comprehensive understanding of a given topic (extended notes, lecture handout, class notes,
recordings), then go through and generate questions and answers that cover each piece of information
you encounter. (So instead of just reading dopamine is implicated in schizophrenia and assuming
youll remember that, write down what neurotransmitters are implicated in schizophrenia? then
answer it. Then what is the evidence that theres too much dopamine action in schizophrenia then
answer it. Etc.)
o Make them so clear you could share it with a stranger. Your mind will love to convince you that it
understands and will remember something when it actually doesnt and wont. Dont trust it! Test it.
o Write this all down. (or type this all up?).
At this point youll probably remember a LOT of what youve studied just by engaging the content in this way.
To remember everything, go through the study guide you just created and quiz yourself on it. Dont just read it,
retrieve it. (see the papers I posted on the power of retrieval learning earlier this year).
Better yet, do it with a knowledgeable study partner. Your gaps in memory will hopefully be non-overlapping.
Plus its more fun.
Obviously focus on the more important things (like the stuff on the lecture handouts, or the stuff we spend half
a lecture talking about instead of the stuff that comes up in one brief sentence). Make a realistic plan for when
you will do the reviewing and the testing, and stick to it with diligence and discipline. Figure out where your
biggest gains are and maximize the utility of your study time, save the minutia for your final go at it.
And if you dont have the time/patience to create your own, using this in the same way (not reading the
answers, GENERATING the answers and then seeing if youre right) will also be helpful. Go through and delete
the answers, and see how you fare.
When youre confident you know something solidly, cross it off and dont rehash it any more. Spend your time
on the things you dont know yet. And DONT pass up things that you dont yet know solidly without extra cues
and prompting. Be rigorous.
Be sure to try out the practice final from last year to see what kind of shape youre in.
Also eat lots of fruits, veggies, and fiber. Get lots of sleep. Get some exercise. They will all do wonders not only
for how you feel, but for how you think. Good luck!
Background from section

My sections are aimed at those who already know the basic background like the basics of natural selection, how neurons
work, central dogma, etc. I was a HumBio major.
These filled-in section handouts will be posted after section. NOT a comprehensive handout of testable material, but it
covers what I think are the most challenging/interesting/ important topics. Sometimes we'll delve into readings if there's
time, but not always. Be sure to do those on your own because there will be a proportion of the test that you won't be
able to answer unless you've done your readings.
Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 2
Contents
Background from section ........................................................................................................................................................ 1
Introduction and Evolution/Sociobiology ............................................................................................................................... 3
Behavioral Genetics .............................................................................................................................................................. 13
Recognizing Relatives ............................................................................................................................................................ 18
Ethology ................................................................................................................................................................................ 21
Advanced Neuro/Endo .......................................................................................................................................................... 25
Limbic System ....................................................................................................................................................................... 29
Reductionism and Chaos....................................................................................................................................................... 31
Sexual Behavior (lecture 1 of 2) ............................................................................................................................................ 36
Sexual Behavior (lecture 2 of 2) ............................................................................................................................................ 41
Aggression I ........................................................................................................................................................................... 45
Depression ............................................................................................................................................................................ 58
Schizophrenia ........................................................................................................................................................................ 61
The Biology of Religion.......................................................................................................................................................... 65
Final Lecture .......................................................................................................................................................................... 68
Introduction and Evolution/Sociobiology

Things that you really need to know (at the end of every extended notes):
-Basic tenets of Darwinian evolution
-The three building blocks of sociobiology
-Understanding kin selection on a mathematical level, to a certain extent.
-The application of game theory to reciprocal altruism.
-The problem of how reciprocal altruism starts.
-How to explain a number of realms of behavior with sociobiological principles.
-An array of critiques of the field.
Our overall goal is to understand how a sociobiologist would make sense of animal behavior.
Pros and cons of categorical thinking

1. Helps you remember and recognize an example of a group.
2. You tend to see members of a group as more similar than they actually are and members of different
groups as more different than they actually are (color perception example).
3. Myopic focus on individual categories (buckets) by leading thinkers of the past has led to disastrous
outcomes
Evolution (change over time) caused by a number of things. We focus on the big one: natural
selection. Requires what three conditions?
1. Heritability (DNA)
2. Variability (mutation)
3. Differential fitness (success in leaving progeny)
Then what happens?
1. Versions that confer more fitness will become more prevalent over time
Sociobiology is the study of the evolution of behavior. What are the three core explanatory pieces
you should be able to apply to a wide range of behavior?
1. Individual selection. "A chicken is an egg's way of making another egg." -Samuel Butler
2. Kin selection/inclusive fitness. "I will lay down my life for 2 brothers or 8 cousins" -JBS Haldane
3. Reciprocal altruism.
Five pieces of evidence for evolution?

1. Observable over past 100 years in short-lived species like staph bacteria & penicillin resistance
2. Fossil record shows tons of intermediate forms
3. Genetic evidence: we share huge percentages of our genomes with our closest evolutionary ancestors,
and less the further you go back in time to most recent common ancestor
4. Geographic distribution of species: relatives are bunched together in space
5. Unintelligent design: vestigal structures like leg bones in dolphins, pyramidal system for finger
movement
In our class: natural selection and sexual selection are different (sometimes opposing) forces.
How do they apply to individual selection?
1. Natural: adaptedness to surviving in the environment
2. Sexual: adaptedness at attracting a mate
How do they apply to kin selection (inclusive fitness)?
1. Natural: Engage in behaviors that allow related individuals to survive and reproduce
2. Sexual: Work to make related individuals seem attractive to potential mates
How do they apply to cooperation/altruism?
1. Natural: non-related hunters cooperating to get game they couldn't get alone.
2. Sexual: cooperatively making a non-relative more attractive to mates
How do you calculate degrees of relatedness?

1. 50% gene-variant similarity with parent or full sibling. 25% with grandparent. 25% with (biological)
aunt/uncle. 12.5% with great grandparent, etc.
2. Each "line" in the family tree that you traverse typically halves the number of genes you share with the
next individual.
Cooperation
1. Kin selection/inclusive fitness
1. Cooperate with relatives, encourage their reproduction.
2. Reciprocal altruism, formalized through game theory with the prisoner's dilemma:
1. When to cooperate vs. defect
What typically characterizes species that demonstrate reciprocal altruism?

1. "Species that are social, long-lived enough and in sufficiently stable groups so that individuals interact with each
other more than once (how else can the reciprocity occur?), smart enough to recognize individuals and, critically,
smart enough to try to cheat at the reciprocity when its possible to get away with it (i.e., to not reciprocate an
altruistic act), and smart enough to spot someone trying to cheat against them." -extended notes
What is Axelrod's famous winning strategy? What does even better under some conditions?
1. Tit for tat. Will lose battles but win wars. Will lose to cheaters, but pairs of TfT will win more than
cheaters ever will.
2. Better with forgiving tit for tat (less prone to signal errors)
3. Pavlov can exploit forgiving tit for tat
What are five examples of TfT or interesting elaborations?
1. Vampire bats (TfT)
2. Stickleback fish (TfT)
3. Gender switching fish who defect if the other defected (TfT)
4. Cowardly lions who are good hunters (different domains of contribution)
5. Huge naked mole rats plugging up holes (different domains of contribution)
Related to kin selection: the greenbeard effect. What is it?
1. Not about recognizing kin, necessarily, but instead just one gene that allows for
1. Recognition of the gene in other individuals
2. Cooperation with other individuals that have that gene
Related to cooperation: rock-paper-scissors equilibrium
1. Actually restraint from competition. Not true altruism.
How does cooperation/altruism start?
1. Founder population cooperates on a basis of kin selection. Then when re-integrated into large
population, they keep "winning the war" and cooperation crystalizes outward or non-cooperation is
driven extinct.
Pair Bonding and Tournament Species

How do we explain imprinted genes?
1. Father's imprinted genes cause a more "selfish" infant that grows a lot, suckles lots of nutrients, etc. at
the expense of the female's future reproductive success. Tournament species males are interested in
mating with many females until they get kicked out.
1. What happens when these go unchecked? Choriocarcinoma.
2. Mother's imprinted genes do the opposite. Slow down growth and nutrient uptake. She's equally
interested in the success of future progeny as much as this one.
1. What happens when these go unchecked? Egg won't implant
3. Exemplify inter-sexual competition via parent-offspring conflict. Higher in tournament species.
How do we explain competitive infanticide?
1. Definitely not for the good of the species!
2. When the average tenure of the head male is shorter than the average interbirth interval in females.
3. Males operating under individual selection: wipe out other infants so mothers can be impregnated (tie to oxytocin
- nursing - fertility suppression - endocrinology foreshadowing), plus less competition for his future offspring.
4. Females coping via individual selection principles: smell of new male causes spontaneous miscarriage because it
doesn't make sense to have an offspring that will be killed. Save on pregnancy costs and get pregnant with the
new male. Female still has 50% genetic interest in her offspring whether it's old male or new.
5. Females coping via kin selection: defending their children up to a point (when would they lay down their life?),
also faking pseudo-estrus to fool the new head male into not forcing them to spontaneously miscarry from
harassment.
What are some further behavioral examples explained well by sociobiology?

1. Kidnapping by male baboons (and not kidnapping when high-ranking male just joined the troupe)
2. Relatedness in dominance hierarchies. Females inherit their rank
3. Sex ratios.
1. Males are more "expensive" but high ranking tournament species females will gamble on a son
instead of a daughter. What's the proximate mechanism here? Higher-ranking females have better
nutrition so sons will be more likely to be carried to term.
2. Sex ratios will stabilize over time near 50-50.
4. Paying attention to alarm calls as a function of relatedness
5. Male-male cooperation
6. Instances of polyandry (multiple males leading a harem).
Usually adelphic (by related males). Includes humans (see
traditional Tibetan marriage patterns).
7. Why would you mate with relatives?
1. Share more genes with them so more of your
genes make it into the next generation. Great!
2. But if they're too closely related than recessive
disease-causing alleles are likely to be inherited
and cause disease. Not so great!
3. Where does the "optimal" mating occur, according
to the Helgason "Kinship and Fertility" reading? 3rd
or 4th cousin matings produce the most fertile offspring.
8. How do chimps vs. baboons differ in which gender leaves the troupe? What consequences does that have?
1. Baboons: males leave the troupe. Females stay and are more related.
i. Males kill each other more
2. Chimps: females leave the troupe. Males stay and are more related.
i. Males band together and often kill neighboring males. This is protowarfare and genocide.
Group selection. Is it valid? What version is invalid?

1. Not for the good of the species.
2. Yes multi-level selection.
a. Founder populations evolve cooperation based on kin selection, and can then outcompete other groups
they are re-integrated with.
b. Situation of A<B but AA>BB.
c. Parochial altruism is the phenomenon of cooperating with an in-group against an out-group, regardless of
kinship. Like WWII.
What are some common patterns of human behavior across cultures and time?
1. Males more violent than females
2. Hierarchical systems
3. Emphasis on kinship
4. Polygamy (most cultures contain polygamy; most individuals within those cultures practice (serial) monogamy)
What are four criticisms of sociobiology?

1. Sociobiology says behaviors are heritable.
a. Criticism: What is your proximate mechanism? Where's the gene? What protein does it code for?
That's the real basis of evolution.
2. Sociobiology says every social behavior is an adaptation.
a. Criticism: This is the adaptationist fallacy that everything is adaptive. You're making up just-so
stories! What about spandrels?
3. Sociobiology says that evolutionary change happens continuously in small incremental steps - gradualism.
Evolution, not revolution.
a. Criticism: What about punctuated equilibrium? Fossil record shows periods of stasis and periods of
rapid change. Tiny adaptations don't make a difference.
4. And political criticisms. "Oh the conclusions you draw scientifically just happen
to justify the hierarchies and inequities our society faces and which you
(Southern, white scientists) benefit from."
Example Exam Questions

- Filling in prisoners dilemma payoffs
- Giving example of real-life prisoners dilemma situation
- Predicting traits (including imprinted genes) for tournament vs. pair bonding species
- How would a sociobiologist justify the existence of parent-offspring conflict over

breastfeeding?
- Name a non-human primate in which female exogamy occurs and what this might have to do
with war-like behavior.
Well be covering the two molecular genetics lectures this time. And the two behavioral genetics lectures next time. And
then ethology and recognizing relatives after that. My sections wont spend much time reviewing the introductory
neuroscience, introductory neurology, and intro to sex lectures which will be done by the TAs next week.
Things to Know
1. How sociobiologists think of the evolution of a trait, and how molecular biologists do so.
2. Basics of DNA, RNA, protein sequence, structure and function.
3. Classical mutations (point, deletion, insertion), how they are the engines of microevolutionary change and sociobiological ideas about
gradualism.
4. How microevolutionary change can relate to behavior.
5. The basic idea of punctuated equilibrium, and the critiques of it.
6. Why it is that a gene doesnt decide when it activates and directs the construction of a protein, and the role of the environment in this
process instead.
7. The basic facts about exons, alternative splicing, promoters, transcriptional networks, transposons.
8. The macroevolutionary consequences of changes in any of these realms.
9. Molecular support for the idea of stasis.
10. Challenges to the central dogma view of genetics and genetic determinism.
Review
1. Proteins are made of amino acids. The sequence of amino acids determine the shape (and therefore the function)
of the protein. Amino acids are coded for by DNA. DNA is a gigantically long molecule with four different bases,
"letters." Three bases next to each other are called a codon. One codon is read to create one amino acid.
2. Proteins serve tons of roles in the body; almost everything interesting is a protein (enzymes, neurotransmitters,
transcription factors, receptors, other signals).
For our purposes, what is the central dogma of life?

1. Information flows from a unique DNA sequence (a gene) to an RNA sequence to an amino
acid sequence.
2. By extension, one gene specifies one protein which has one shape and therefore one
function
And what is the main challenge to the central dogma in this course?
1. That one stretch of DNA can actually lead to many different proteins (through alternative
splicing)
2. (also retrotranscription in viruses from RNA --> DNA)
3. (also one protein can take on multiple conformations and serve different functions)
What are the molecular bases for the three tenets of evolution by natural selection?
1. Traits are heritable: you get your genes from your parents, and them from their parents, and so on.
2. Variation: different alleles (versions of genes) code for slightly different proteins that serve the same function.
3. Differential fitness: those different versions might do their protein job slightly better or worse, depending on the
environment in which they're working
What are the three types of mutations in classical genetics?

1. A point mutation when a single nucleotide is copied differently (incorrectly) between a mother cell and a daughter
cell.
a. Can be a neutral mutation thanks to the redundancy of the codons. That is, multiple sets of 3 DNA bases
will code for the same amino acid. So if the point mutation changes from one codon into a different but
reduntant codon, it's a neutral/silent mutation.
2. An insertion mutation leading to a frameshift.
3. A deletion mutation leading to a frameshift. Deletions can also be of entire genes.
*What do we mean by microevolutionary vs. macroevolutionary change?

1. Micro: a change in a single protein that affects a single protein and the downstream effects of having a differently
shaped protein.
2. Macro: a change in something (promoter, transcription factor, splicing enzyme, transposase, etc) that produces
far-reaching changes in the way many proteins are made or when they are expressed.
Four examples of a microevolutionary change having a big impact on behavior?

1. Phenylketonuria (PKU)
2. And two examples related to testosterone?
a. If your T receptors are mutated and don't function, you are genetically XY male but
have female appearance because your body doesn't respond to the presence of T.
This is testicular feminization syndrome.
b. Enzyme that makes T is mutated in early life, but doesn't hold back T production at
puberty in populations in New Guinea and Dominican republic. Guevedoces: what
are thought to be "girls" (but are actually XY) develop male secondary sexual
characteristics around puberty when T kicks in.
3. And an example related to anxiety?
a. The benzodiazepine receptors come in different versions based on subtle mutations.
b. The better the receptor binds BDZs, the less anxious the individual will be. If they're
very poor BDZ binders, the individual will have an anxiety disorder.
How can micro mutations tell you about evolutionary ancestry trees?
1. We share "the gene" for many proteins with distantly related species (a significant percentage of our genes are
shared with bananas, for example).
2. But as species evolve and diverge, differences accumulate in our genes so that the proteins of very distantly
related species have many differences between them while the same proteins in very closely-related species have
very few differences between them.
How do you know if a protein has undergone positive selection or negative selection?
1. Take a protein product that is shared between species, like a serotonin receptor shared between dogs and
humans.
2. Look at the DNA sequence that codes for that protein. Just by random chance we expect, say, 1/3 of the
mutations (differences) between those two DNA stretches to actually code for a different AA (amino acids),
resulting in a slightly different protein.
3. However, if 3/4 of the mutations coded for different AAs, this gene has undergone positive selection and the
differences that have accumulated were the result of selective forces over time selecting for a new and better
version of that gene.
4. If say 1/8 of the mutations coded for different AAs (that is, more of the mutations were neutral than you'd expect
by chance), then that gene has undergone negative selection/stabilizing selection, meaning that it is very
conserved among species because slight changes have been selected against.
If that's still confusing, here's another explanation from last year:
You start off with a gene in an organism at time T1.
After a long evolutionary time period during which the gene has undergone numerous mutations, you come
back and re-examine the gene, which is no longer identical to its original form.
You're comparing the newer version of the gene at time T2 to the original gene at time T1 and looking at the
mutations that have happened.
Based on the type of mutations (silent/neutral or consequential) that you see, you can know whether this
gene has faced selective pressures or not, and if so, what type of selective pressure.
o If nothing interesting has happened and those genes have not undergone any particular selection
pressures, you'd expect 1/3 of the mutations to be consequential (due to the mathematics of the
DNA-amino acid link).
o But if significantly more than 1/3 (like 90%) of the mutations are consequential, the gene has
undergone positive selection because having so many more consequential mutations (ones that
actually make a difference in the protein formed) than would be expected by chance means that, in
order for this gene to have evolved this way and exist in its present form, that large number of
consequential mutations must have been selected for.
o And if significantly fewer than 1/3 (like 5%) of the mutations are consequential, the gene has
undergone stabilizing/negative selection (pressures to keep the gene exactly how it functioned
originally). This is because when consequential mutations happened along the line from T1 to T2,
those changes were selected against and the original genetic sequence is highly conserved.
What is the 95% of DNA that doesn't code for proteins?

Promoters, repressors, and "junk DNA" which we don't know much about
The longer the genome in a species, the greater percentage of genes tat code for TFs
How do you know when to express certain genes?

1. Can be answered at many levels.
a. When the transcription factor (TF) binds to the promoter
b. When the intra-cellular environment signals transcription via TFs
c. When the inter-cellular environment signals transcription, e.g. via testosterone
d. When the inter-organismal environment signals transcription, e.g. a mother smelling
her newborn.
Overall, this is the concept of if-then clauses.

1. Example: if you smell your newborn baby, then express genes related to nursing.
What's 1 molecular mechanism and 1 example of epigenetic regulation?

1. Chromatin packing patterns can be set for life.
2. Examples include
a. Metabolic programming during the Dutch Hunger Winter
b. Stress reactivity in rats as a function of licking and grooming from the mother
What do transposons do and where do we see them play out in nature?

1. Transposons are mobile bits of DNA clipped by transposases and inserted into random
parts of the genome
2. Originally found by Barbara McClintock in corn. Often found in plants as a stress
response to come up with a novel solution under dire circumstances that plants can't run
away from.
3. Also seen in neuronal wiring of mammalian brains. Significance: the organ having MOST
to do with behavior is LEAST deterministically goverend by one set of genes. A lot of noise
in the system and less of a role for a deterministic view of genes.
4. Also seen in parasites like the trypanosome worm which uses transposons to reshuffle its
surface signal proteins to evade immune defenses.
5. Also seen in the immune system of mammals.
What's the basic idea of Punctuated Equilibrium (PE) and what's the evidence for it? How do
gradualists respond to those claims?
1. PE is a model that explains evolution. The idea is that there are long periods of stasis (the equilibrium part) in
which nothing exciting really changes and then periods of saltation (the punctuated part).
2. Paleontological evidence: we see in the fossil record what looks like saltatory change and periods of equilibrium
a. Gradualist ("creeps", as opposed to PE "jerks") say the fossil record is incomplete and
maybe it's gradualist if we had more data.
b. Gradualists also say that "sudden" change for PE folks is plenty of time for
sociobiologists to examine evolution of behavior in what they'd call a gradual
manner.
c. Gradualists also say that PE folks are only looking at morphology or the way things
are shaped. You get very different behaviors based on neurons and brains, and you
can't directly examine those with paleontological evidence.
d. Gradualists in the old days also demanded to see molecular mechanisms for these
changes. See below for response.
What's the molecular mechanism of PE changes?

1. Mutations in the regulatory regions of genes. We call these mutations
macroevolutionary.
a. These include: promoters, repressors, TFs, splicesomes, and transposases.
Transposon action itself (even when not mutated) can change entire if-then
sequences.
2. And multiple genes can be regulated by one TF or one promoter
3. And any given single gene probably responds to multiple TFs and promoters.
So we have networks of genes and when you disrupt the controllers of those networks,
their regulators, you can produce radically new if-then clauses. So a new environmental
situation can trigger an existing pattern, OR the same environmental situation can trigger
a new pattern if you have just small mutations in any of these regulatory sequences.
What about the mechanisms for the stasis part in PE?

The price of complexity of everything we've seen means that these small changes that have big amplfied effects
are often going to have very deleterious effects, and will not be selected for. So we'll see a lot of stability in these
systems.
We'll see the saltations at periods where there's an evolutionary bottleneck, like there was with cheetahs.
How can you get multiple proteins from one gene?

Alternative splicing. Can rearrange the exons and selectively keep some of them for translation into protein.
That's how we can have 20,000 genes but also have 100,000 different proteins.
3. This means any given exon may end up in many proteins. Mutate that one exon and you can amplify that
mutation to affect many proteins (overlapping genes).
How did the prairie vole example show these principles?

1. A mutation in the promoter for vasopressin receptors changed where the repressors
were.
2. In monogamous voles the vasopressin receptors are expressed on dopamine neurons.
3. In polygamous voles the vasopressin receptors are NOT expressed on those dopamine
neurons. So when these voles mate and vasopressin is released, the polygamous ones
aren't reinforced to be monogamous in the same way the monogamous ones are.
4. This emphasizes that it's not the protein (the vasopressin receptor) itself that's changed,
but rather the context in which that gene is expressed.
Three (simplistic) examples of novel if-then clauses that you could explain with the above
mechanisms.
1. If it's dry out, then retain water --> if it's dry out, then mate. (seasonal mating).
2. If you smell a relative, then nurse them --> if you smell a relative, don't mate with them. (incest avoidance).
3. (or you change the if part): if you are secreting glucocorticoids, then suppress immunity --> if you are secreting
progesterone, then suppress immunity. (maternal immunosuppression during pregnancy).
How does the existence of duplicated genes/copy number variants give us more explanatory wiggle
room when we're looking at genetics and behavior?
1. So you can have duplications of an entire gene.
a. One can get knocked out or mutated into oblivion and you're still okay
b. You can also use these duplicates to double the amount of protein you produce given the same promoter
activation.
c. So one can mutate a bit and the other can serve as a backup.
2. Examples:
a. You see a lot of copy number variants in the genomes of those with schizophrenia
b. Steroid hormone receptors
Who wins in the end? The gradualist creeps or the PE jerks?

1. Both! Yay.
2. Gradualism:
a. Molecular evidence: small point mutations CAN produce slight changes in protein function that can be
selected for.
b. SOME fossil records show evidence for gradualism
3. PE's evidence is all laid out above. Also:
a. We've seen punctuated events in our lifetime. Four examples
i. Siberian foxes that look like dogs
ii. Chicago rat skins show rapid change since 1850
iii. Human populations exposed to western diets undergo almost a bottleneck of diabetes
iv. Bacteria evolving antibiotic resistance
4. And they can both happen simultaneously in different realms.
Example exam questions

Behavioral Genetics
Things to know for behavioral genetics:
How behavior geneticists, sociobiologists and molecular biologists differ in their intellectual approach to detecting
a genetic influence on behavior.
How behavioral geneticists think about behaviors running in families as a function of relatedness, and the
criticisms of this.
The various approaches dissociating sharing biology with an individual and sharing environment with an individual
(i.e., twin studies and adoption studies), and the various pitfalls of these approaches.
Approaches in which one studies behaviors that occur in the absence of environmental influences.
To understand the strongest critique of that approach, namely prenatal environmental effects.
The ways in which genetics that don't follow classic Mendelian rules become relevant.
How the behavioral genetics and molecular genetics approach can be combined to find markers for actual genes.
What heritability means.
Some sense of where chance comes into this.
What are the major approaches used by the behavioral geneticists? What are the criticisms of
these approaches?
Remember they're all about teasing apart genetic and various environmental influences.
Universality, shared among family, and shared as a function of relatedness.
a. Saying traits more shared with closer relatives must be due to the more shared genetics.
b. Criticism: Genetics and environment tend to correlate well within families as a function of
relatedness
c. Criticism: you're not actually controlling for environment because your pre-natal maternal
environment is crucial (Dutch Hunger Winter, epigenetics, etc.)
MZ vs. DZ twins.
a. Criticism: even among MZ twins you have
i. Splitting before day 4 two separate placentas (dichorionic) and two amniotic sacs
ii. Splitting between day 4-7 one placenta (monochorionic) but two amniotic sacs
iii. Splitting after day 7 one placenta and one amniotic sac
b. Criticism: MZ twins are also treated more similarly than DZ twins
Adoption studies. Saying that traits more shared with closer relatives must be due to more shared genetics
because the environment is random and not shared.
a. Cross-fostering in animals
b. With MZ twins separated at birth
c. Compare MZ and DZ twins separated at birth
i. Criticism: adoptees are placed non-randomly
ii. Criticism: you're going to have pretty small sample size with these very unique cases
iii. Criticism: again, environment starts at conception, not at birth
Behavior in the absence of environmental influence
a. Social smiling in congenitally blind babies and babbling in congenitally deaf babies
b. Lab rats 100 generations away from ever seeing a cat are still averse to cat pheromones
What 3 important things happen in the pre-natal environment?

o Circulating hormones (from mother and from rat siblings strung up on the same circulatory
chain)
o Glucocorticoids and other stress hormones. High exposure to these brings, as an adult,
smaller brain, lower capacity for learning, more tendency towards
anxiety/hypertension/diabetes. Sheesh!
Leads to epigenetic effects of inability to shut down stress response thanks to smaller
hippocampus
o Maternal and sibling estrogen influences also influence subsequent development (earlier
puberty, etc).
o Nutrition and metabolic programming
o Prime example of epigenetics (non-mendelian inheritance of traits, even multi-
generationally, that has nothing to do with genes - are not heritable traits).
o We also see pelvic arch size evolutionary battles with Massai malnutrition
o Learning (mother's voice)
Some would say maternal and paternal genetic contributions are equal, and that mom also gives
the prenatal environment.
How would you then explain any differences you saw in behavior as shared more with mom?
Due to the influence of the prenatal environment. That's how we can control for it.
But what complicates that assertion? In what ways is mom more than just 50% genes + prenatal environment?
Paternal uncertainty
Mitochondrial DNA
Imprinted genes
TF inequality and Lamarkian inheritance
And say we do discover a strong genetic component for something like extroversion. What might
the genes actually be influencing? 3 examples:
Something indirectly related to extroversion, like attractiveness. These are indirect genetic effects.
Another example: high heritability for political affiliation may have to do with the genetics of ambiguity tolerance
Aggression in rats also seems highly heritable. Not actually genes for aggression! About pain tolerance
thresholds.
How do behavioral geneticists hone in on actual genes?

Find genetic differences, then look for differences in behavior.
To find genetic differences in order of awesomeness:
o phenotypic marker linkage <
o protein marker linkage/protein size <
o RFLPs <SNPS <
o QTLs <Microarrays
Drawback: it's about identifying covariants in the genes with the disease, so it's a statistical relationship
and often doesn't give 100% certainty.
Drawback: you do all this work in a family, but then in a different family they'll have different markers.
So multiple genetic routes to a disease.
Drawback: even knowing the exact gene, it's usually not 100% deterministic
Or the reverse: find variations in genes and then study "where the light is" to figure out its effects.
What three examples do we have?
Vasopressin receptor variants. Not just voles, also humans! The "monogamous" promoter
version makes for more stable marriages and greater facial expression-reading ability in
humans!
Variants in BDNF in humans predict risk of anxiety and amygdalar metabolic rate (same with a
neurotransmitter called NPY).
Variants in dopamine and serotonin receptors and risk-taking
Criticism: Looking where the light is. By looking where there is an expected effect, theyve eliminated the chance
to find an unexpected effect.
Criticism: multiple genes affect the same outcome behaviors sometimes. Therefore one single gene variant
probably has very small effects. You won't be illuminating complex human behavior.
What does heritability tell us?

Heritability DOES tell you the degree to which the variance of a trait is influenced by genes.
Heritability DOES NOT tell you the degree to which a trait (the average of the trait) is influenced by genes, or how
much a trait "is genetic."
The fact that humans usually have 10 fingers reflects the fact that this trait is inherited. But cases where humans
have fewer than 10 fingers involves 0% heritability.
How do we know if something is highly heritable?

Look at the variation in a trait and ask yourself did that variation result from differences in genes or differences in
the environment? If it's differences in genes then it's highly heritable.
For traits that are highly heritable, then knowing the gene will give you huge predictive power over the variation
displayed in your trait of interest.
For traits that are not highly heritable, knowing the environment or some other factor will give you more
explanatory power over the variance in your trait of interest.
Which of the following show high heritability?

And for one more complication, what role does chance play in the development of an organism?
Particularly in the splitting of cells, brownian motion (unpredictable, probabilistic movement of atoms and
molecules) will not cause equal 50-50 splits of all the TFs and hormones and other cytoplasmic things.
Key examples - know the details, their significance, their criticisms. What do they illustrate? Why
are they included?
Benbo and Stanley's gender differences in math from the CTY kids
At first concluded it was a reliable (genetic) sex difference that males outperformed
females at math because their mathematics environments were "identical"
But the different sexes are treated differently. And upon retesting 30 years later the
differences are small to disappearing (too short a time for strong genetic shifts). AND
looking across countries, the smaller the gender gap in social/political/economic terms, the
smaller the gender gap in mathematical performance.
But the difference does seem to hold true that males outperform females on average and
not very hugely on spatial tasks. And females also seem to consistently outperform males
on average and not very hugely on verbal tasks.
Kety's schizophrenia adoption studies
The Dutch Hunger Winter
Phenylketonuria and gene/environment interactions
Depression and gene/environment interactions
MAO variation and aggressive behavior gene/environment interactions
Take-Home Points
Environment does not begin at birth; it begins at conception. And supposedly subtle prenatal effects can be
anything but subtle.
Most interesting human behavior is not about deterministic single genes. Many genes are involved in almost any
behavior, plus they're all interacting with the environment.
It is meaningless to talk about what a gene does, only what it does in a particular environment. The more you
know about genetics, prenatal environment, early childhood experiences, societal context, stressors, etc., the
more predictive you can actually be about important outcomes (like risk for depression).
But genes are of course important to behavior. Gene X Environment = Behavior just as Width X Length = Area

Why do traditional scientific approaches under-estimate the role of environment in determining a behavior?
Define heritability in one sentence (2 points)
Seymour Kety examined incidence rates of schizophrenia in a large number of cases of early adoption in Denmark
in the 1960's. A simplified summary of the outcomes is shown below.
Percentages in the table above represent the

incidence rate of schizophrenia for each
context (for example, 1% of all the
individuals with NON-schizophrenic
biological parents and NONschizophrenic
adoptive parents have schizophrenia).
Briefly describe how analyzing these groups
might lead to a dissociation between genetics
and
environment. (2pts)
Environment does not begin at birth.
a) Give three examples of this principle from class. (6 pt)

Prenatal stimulation and learning mom's voice
Prenatal stress and later stress reactivity
Prenatal malnutrition and later thrifty nutrient phenotype
Drug addiction can occur in the womb
Recognizing Relatives
Things to know for scientific findings:
What scientists mean by stating a degree of confidence about a finding.
The difference between the consistency of a difference and the magnitude of a difference, as played out on the
population level.
Ditto on the individual level.
And know for Recognizing relatives
Why it makes sense to be able to recognize relatives.
How the MHC makes instinctual recognition of kin possible.
What sorts of sensory cues can be used for kin recognition.
Examples of cognitive derivation of kin in non-human species.
Non-cognitive modifiers of kin recognition in humans.
And know for Ethology
The contrasting intellectual traditions and styles of behaviorism versus ethology.
What a FAP is, examples, including human ones.
How ethologists approach the issue of adaptation, in contrast to the approaches of other disciplines weve heard
about.
How ethologists go about studying and identifying releasing stimuli.
Examples of releasing stimuli in different sensory modalities.
Some examples of neuroethological approaches.
What's the difference between statistical significance and functional significance/importance?

Stats is just about how consistent a finding is, how unlikely it is to be caused by chance. Is the difference observed
"real" or accidental? Larger sample sizes make for greater statistical significance.
Actual importance of a finding, or effect size, is how much of a difference did you find? Does it actually make any
difference in the real world for the way we think and make assumptions and behave?
Generally, the smaller the effect size is, the larger your sample size needs to be to prove that it's statistically
significant.
There's also usually huge overlap and a lot of variability with big wide bell curves for most of these findings that
are not very important.
o So say you know ethnicity A is, on average, 1/4 inch taller than ethnicity B, on average.
o Pick out any given person of ethnicity A and any given person of ethnicity B. Knowing only ethnicity, how
likely are you to predict which is taller? The closer to a 50-50% chance, the less important the difference is.
Is a finding important?
o How much of the variability in a population is explained by the finding? If not very much then it's not very
important. Similar to heritability and variation.
o If knowing what's true about groups gives you huge predictive power for individuals of those groups, then
that's a very functionally significant (important) finding.
So this is the shortcoming of individual prediction based on overlapping group data.
Recognizing Relatives
Why is it important to recognize relatives? 4 things
Expressing parental behavior like nursing or paternal investment. Kin selection relies on kin
recognition.
To detect defectors! Like recognizing when some other bird has left you with her eggs, or some
other slime mold strain is taking over the fruiting body.
Mating choices - 3rd cousins all the way!
Cooperation and aggression
Example: Dominance hierarchies in baboons (this is also evidence for vocal recognition of other family lines in
baboons)
In what ways do species recognize relatives?

Cell-cell recognition.
o Like in social bacteria using a distinctive surface protein
o Like in cooperating sperm who swim faster when clumped together. No clumping with foreign sperm!
Innate recognition
o This is an instinctual, innate system. Note: cross-fostering isn't going to work here. You can't fool innate
recognition!
o Like rodents who prefer the smell of siblings that they've never met. Can also recognize degree of
relatedness instinctively. Requires what hormones on board? vasopressin and oxytocin.
o How does it happen? Olfaction and pheromones. Requires oxytocin and vasopressin on board to do this
recognition or else you have social amnosia.
o What are in these pheromones that distinguish self from non-self? MHC proteins. The more distantly
you're related to somebody, the more different your MHC proteins are.
o Facilitated by neurogenesis in the olfactory system during pregnancy in rat mothers, as a result of high
prolactin levels.
Imprinting on a sensory cue
o When mothers recognize infants by imprinting some logical cue. The capacity to do so is innate, but the
specific cues that tell them who relatives are come from the environment. Things like:
Vaginal fluid, amniotic fluid, milk, saliva, scent gland markings, response to mating calls
And siblings and cousins can use these same traits as second-order cues to kin recognition. Rules like
"siblings smell like mom's amniotic fluid" or "cousins are the birds who sing songs somewhat similar to
mine"
o Or vice versa: when baby ducklings imprint on the first big moving thing they meet after birth,
thereafter treating it like mother
Cognitive derivation of kinship
o Not by simple sensory rules, not by cell-cell recognition, not by innate mechanisms.
o It's thought and recognition. Examples:
If I remember giving birth to this individual, it's my offspring.
If I spent my childhood with somebody, they're probably a sibling (humans). Shown by kibbutz studies
and Taiwanese arranged-marriages-from-childhood.
Two more:
Face recognition (appearance similarity) in humans (and sheep!)
If I mated with this individual's mother a high proportion of the time she was in estrus,
it's probably my offspring so I'll be paternal. Higher primates and sunfish can similarly
do this.
In humans
o We have a special structure, the fusiform "face area" of the cortex in the brain recognizes faces.
o In what disease does the fusiform area not function in a typical manner?
Autism. Just as likely to light up for a picture of unknown vs. familiar faces.
o We have elaborate cognitive understandings of relatedness.
o We don't do instinctual smell recognition, but mothers and babies learn each other's smells soon after birth
(fathers don't).
o Infants can learn mom's voice in utero (imprinting on a sensory cue)
o Since it's so fluid and subject to error and cognitive, we can have both pseudo-kinship (bands of brothers in
the army) and pseudo-speciation (making others seem so non-related as to be of a different species
entirely)
o In what 3 ways have we seen humans "fooled" into thinking people are relatives who are not, or vice versa?
Kibbutz studies and Taiwanese traditional marriages
German brother-sister couple example: it can't be innate or they would have figured it out
earlier!
Ethology
Where did ethology emerge from?
A philosophical psychology of the early 1900s led to behaviorism with
Watson and Skinner.
o Behaviorism is all about stimulus-response, reward-punishment,
and how these lead to observable, quantifiable behaviors. It's
about radical environmentalism: almost nothing innate; all about
the environmental shaping that explains behavior and life
outcomes.
o Behaviorists were really in to reinforcement theory.
Positive Increase likelihood of repeating a
reinforcement behavior
Positive punishment Decrease likelihood of repeating a

behavior
o Very into simplified, clean experiments in highly controlled laboratory settings. Uniformity.
Then we get an ethology backlash which is much more about what?
o Variety in nature
o Interviewing animals in their own language
o Making sense of animal behaviors only in their natural context/environment
Ethology is then about a few basic questions

What does the behavior look like?
We look at fixed action patterns (similar to reflexes and instincts, but more elaborate).
o A small, coordinated set of movements with an interconnected social meaning. An innate behavior.
o Performed without prior experience but experience can shape the FAP (learning can happen)
o It's usually triggered by a releasing stimulus
o Examples?
Squirrel nut cracking.
Human smiling and other human facial expressions.
Fear grimace in macaque monkeys in response to a photo of a menacing superior macaque's facial
expression.
Vervet monkey alarm calls. Infants can make the calls (they're innate FAPs) but learning shapes when
they give the calls to the appropriate context.
Fear response to the visual cliff
There are other, non-FAP behaviors that ethologists study and make sense of, but FAPs provide a good example
for understanding the later questions of ethology.
What is the adaptive value of the behavior? Why do they do it? What happens in its absence?
Sociobiologists framed in terms of reproductive success, of course. Ethologists are more about doing experiments
in the field to literally see the adaptive value in nature.
Example: FAP of gulls turning over egg shells, speckled side up. They carry it out for speckled cardboard,
etc. This provides camouflage from raptor predators and white side up makes them easier
predatory targets.
Example: waggle dance of bees. A FAP in response to finding food. Useful in that it directs other bees to the food.
But how do you know? Get in there and do ethological experiments! Rotate the hive so the directional information
is opposite. Or switch where "the sun" is by having a bright light in a different direction.
What in the external world caused the behavior?

This is the realm of releasing stimuli (RS): the stimulus in the environment that triggers a FAP.
How do we know what the RS is? Example of the red dot on bird beaks (the RS) that baby birds peck (the FAP)
o Substitution: eliminate the RS and see if the FAP occurs (paint over the red dot)
o Replication: create the RS in isolation and see if the FAP occurs (paint a red dot on a piece of cardboard)
o Superstimulation: take the RS and amplify it hugely (paint a GIANT red dot)
Often a RS triggers a FAP which is in turn a RS for a subsequent FAP in the first individual, and so on, especially
around courting and sex.
Also RS come in many modalities. Like what?
o Auditory RS: roaring stags cause ovulation. Humans and others have higher-pitched female vocalization
around ovulation.
o Visual RS: turkeys and the experiments teasing apart what triggers their mating behavior. And baby-ness RS
(big eyes, shortened muzzle, round big forehead).
o Olfactory: hamsters and other rodents. And humans (the fear-sweat activates amygdala, and the sad-tears
dampen sexual arousal examples).
o Electrical: electric fish with electric FAPs
o Vibration: spiders with their webs, termites in the wood, and elephants with their feet
Special case of Harlow's rhesus monkeys
o Give them two "mother figures"
Cold wire mom gives milk
Cloth mother is warm and comfortable
o Classical learning (from behaviorists) would predict the milk rewards would cause attachment. Prediction
was violated because the infants preferred the warm cloth mom all the time except when feeding.
So attachment FAPs from the infants were due to comfort RS instead of food RS.
What is the internal biology that produced the behavior? This is neuroethology.
Instead of the behaviorists who treat the brain as a black, unobservable box, ethologists wanted to know what
was going on once the tools were available.
They called the steps between an RS and a FAP, the innate releasing mechanisms. Now they call the study of
these mechanisms, neuroethology because it's diving in to the neural level.
What have they found? 3 examples
o 1: How does the lordosis reflex work?
It's a FAP of exposing female hamster genitals in response to flank pressure and is
mediated by estrogen (she only does it while ovulating).
Estrogen causes the entire pathway of the FAP to work (tactile receptors feed the
brain, brain computes the signal, sends signals to the muscles, etc.)
o 2: Subliminal presentation of fearful faces is an RS for complex physiological fear response
in humans (resulting in amygdala activation).
o 3: Birds and their mating behavior can have accelerated courtship times in response to
climatic changes (mediated by reproductive and stress hormones which they're studying in
wild birds).
How does learning play a role? How did ethology provide a backlash to behaviorism in the realm of
learning?
Back to behaviorists. Whats their view of traditional learning?
o Rewards lead to more of a behavior
o Punishments lead to less of a behavior
o Takes many repetitions to do classical conditioning
Ethologists like learning in contexts that defy behaviorism
o Imprinting like with baby geese. Major learning occurs without rewards or punishments.
This is one-trial learning happening within a critical window for imprinting. Defies all
manner of behaviorism.
o Prepared learning like with the Sauce Bernaise syndrome. You are prepared to learn
associations between food and belly aches than between sound and belly aches, even if the
sound stimulus is much closer to the belly ache experience.
o We have innate predispositions to certain kind of learning
Ex: bees with learning smells better than visual stimuli.
Ex: humans are easier to condition to fear snakes and spiders.
Ex: humans spotting animate over inanimate objects.
o General point: understanding the appropriate context to display a behavior is huge. There's innate behaviors
(defying behaviorism) and they're shaped in very non-behaviorist ways.
Ethologists also like learning in surprising contexts. Like what?
o Mother primates learn how to be better mothers over time. How do we know? Later offspring do better
than earlier and mothers with "aunting" experience have better success with their first borns.
o Meerkats teach their kids how to hunt scorpions. Gradual introduction of more elaborate scorpion-hunting
techniques.
o We also see culture, transmission of traits down generations in certain groups.
Then cognitive ethology
Understanding animal thought processes
Griffin studying animal awareness. How do you test this? The mirror test.
Studying theory of mind (that others have different minds and know different thinks) in chimps and corvids. How
did they test this in chimps? The transparent or opaque screen and taking food out from under
the high-ranking chimp's nose.
Also evidence of theory of mind:
o Chimps and dogs can tell purposeful vs. accidental behavior
Even bees have flexible cognitive strategies. Shown by what? Bee dance signals that there's food where it
makes no sense that there's food: in the middle of a lake.
They have numerosity and as well
Example questions
Describe the patterns present with vervet monkey alarm calls. What do they teach us about core principles of
ethology?
o They are FAPs learned at birth but shaped by experience to be emitted in response to appropriate releasing
stimuli. Vervet monkeys also have flexible cognitive strategies and know not to listen to young,
inexperienced vervet monkeys.
Describe the marital patterns associated with Israeli Kibbutzs. What does this tell us about human kin
recognition?
o Children form the same kibbutz don't go on to marry people from within their kibbutz. Shows they think of
their kibbutz-mates as pseudo-relatives; their cognitive strategy has been fooled.
Key examples - know the details, their significance, their criticisms. What do they illustrate? Why
are they included? (these are all ethology)
Nut cracking in squirrels
Vervet monkey predator alarm calls
The waggle dance of bees
Speckled egg shells
The red dot on beak as a releasing stimulus
The lordosis reflex and its adaptive value
Mother primates learning how to mother
The sauce barnaise syndrome and one-trial learning

The dot test in chimps/elephants
[My sec ons skipped the introductory neuro and endo lectures as they were
aimed at people who have taken the Bio or HumBio core. ]
Advanced Neuro/Endo
Things to know for advanced neuro/endo
Dale's Law #1 and its violation
That there are numerous molecules relevant to exocytosis, opening the way for more steps that can differ among
individuals.
The possible informational purposes of multiple neurotransmitters in a single vesicle.
What is peculiar about retrograde neurotransmitters, and their uses.
Neuromodulation, as a concept
How multiple factors can regulate the number and function of a type of receptor; examples.
Some additional forms of unconventional communication
Things to know for limbic system
Yes, know the Papez circuit (i.e., the structures that make up the limbic system, and their interconnections).
Have a broad sense of the triune brain schema, and the intersection between the limbic system, and the
endocrine/autonomic nervous system at the hypothalamus.
Difficulties in figuring out limbic function.
Soundbites about the function of each area. Far more detail to come for some of them.
Big point: this is all about complexities allowing for individual differences.
Key to abbreviations:
AP Action Potential
NT Neurotransmitter
Hyp Hypothalamus (brain structure)
Pit Pituitary (brain structure)
CRH Cortocotropic Releasing Hormone (from hyp to pit)
ACTH Adrenocorticotropic Releasing Hormone (from pit to adrenals)
GCs Glucocorticoids (stress hormones from adrenals to body)
VP Vasopressin (hormone from pit to body and from hyp to pit)
OT Oxytocin (hormone from pit to body)
Advanced Neuroscience
What complexities do we have at the level of the action potential?
Dale 1: all axon terminals receive AP. Wrong!
Differential spread/shunting of APs
o By regulating density of channels at branch points
Dendrites regulate the input power: not all dendrites equally influential on a downstream AP
Shifting axon hillock to regulate propensity to fire an AP
Vesicle release enzyme complexities: synaptotagmin on vescicle surface, receives Ca++ and triggers many
cascades
Exocytotic pores, not just fusion of vesicle with axon terminal membrane
What complexities do we have at the level of NTs?

Dale 2: one NT per neuron. Wrong!
Multiplicity of NTs
o Different speeds of action: fast excitation followed by slow inhibition

o Therefore multiplicity of receptors for different NTs
Autoreceptors doing bookkeeping

o Sometimes using the second NT as a marker of how much first NT released
Retrograde NTs
o ATP, adenosine
Lateral NTs
o Gasses like NO
What NT receptor complexities do we have?
Not just excitatory, but also inhibitory receptors
Outward ion flow
Multiple receptors for the same NT: non-NMDA and NMDA receptors for glutamate giving us non-linearity in
excitation.
o NMDA is threshold-dependent. Non-NMDA is non-threshold dependent (like most normal, well-behaved
receptors)
o The more non-NMDA providing a graded response, the more likely to reach the threshold and trigger the
NMDA receptor to let Ca++ rush in.
GABA receptors with multiple binding sites for benzodiazepines, barbiturates, and progesterone
GCs having differential effects on glutamate
o GC decrease glutamate in hippocampus
o GC increase glutamate in the amygdala
Autoregulation of receptor number. Crucial in neuro and endo.
Multiple subunits and switching subunits
Second messengers acting within the neuron in response to NT binding. Huge realm of variation and complexity.
What complexities do we have at the level of neurons and their connections?
Axo-axonic synapses and creating if-then clauses
o GABA works this way. Inhibits the excitation of another neuron: neuromodulation
Glia with tight junctions and NTs of their own
Transaxonal signaling
Advanced Endocrinology
How do we go about releasing ACTH from
pituitary?
ACTH released in response to CRH, but also
in response OT, vasopressin, epi, and
norepi. These are our multiple secretagogs.
o The non-CRH ones usually
modulate CRH's ability to
cause ACTH release. Like
vasopressin making CRH
much more effective at
triggering ACTH release, while
vasopressin does almost
nothing all by itself.
o Different release profile for different stressors, as received by the hypothalamus.
o These also modulate other hormone release from the pituitary besides ACTH
depending on the stressor, like growth hormone.
On a cellular level: mosaic of cell types in the pituitary modulate each other
o Each individual cell is specialized to release only one pituitary hormone
But each cell's neighbors modulate its release profile with paracrine signaling
o Hypothalamus can shunt releasing hormones down various capillary beds
(side note: vasopressin is released from the posterior pituitary to have effects on peripheral physiology like on the
kidneys. It's also released into the hypothalamic-pituitary portal system where it influences the anterior pituitary)
How do the adrenal glands respond to ACTH?
More amounts of ACTH from pit eventually reach a threshold of peak amount of GC
secreted from adrenals.
But the peak secretion amount continues for a longer time in response to more ACTH.
What do GCs do once released into the blood?
Binding globulin (chaperone proteins) levels determine its availability to act on cells
o Example of gestational diabetes during pregnancy. High estrogen causes high GC binding globulin
availability causes low GC availability causes high GC production due to lack of negative feedback. When
high GC production overshoots, you end up with high blood glucose which is gestational diabetes.
By itself, GCs do nothing to BP. But synergize with SNS input to skyrocket BP.
How does negative feedback work in these systems? 3 ways:
1. Amount of peripheral hormone work as negative feedback in the brain.
o Often not in the hyp itself, but upstream.
2. But it's also about the ratio between hormones sometimes
3. And it's also about the rate of hormone increase sometimes
o Rate often important in short-term feedback
o Amount often important in longer-term feedback
What complexities do we have in how peptide

and steroid hormones act?
Peptide hormones acting on surface
receptors can trigger messenger
pathways that have big downstream
effects deep inside the cell, including
gene transcription which is often
considered only the domain of steroid
hormones.
o Steroid hormones usually act on
intracellular receptors and modulate
transcription.
o But also act outside (like
progesterone with GABA)
o Also sometimes act not on DNA
transcription directly (they can block
TFs and such)
o Also the intracellular receptor can have a cofactor that causes the same steroid
hormone binding to the same receptor (just with or without a co-factor) to have
differential effects on gene transcription.
What hormone receptor complexities (just like NT receptors!) do we have?
Autoregulate receptor numbers in response to stimulation. Low stimulation -> upregulate receptors. High
stimulation -> downregulate receptors.
Switch sub-units to change their efficacy or second-messenger systems
o Many subunits makes for many types of combinations
o Example: glucocorticoid action in the brain. Bind to same receptor, but the cofactor differs.
Hippocampus: cofactor causes GCs to cause less growth factor expression --> neuron atrophy
Amygdala: cofactor causes GC to cause more growth factor expression --> increased anxiety
susceptibility.
Multiple binding sites
Limbic System
What are the three layers of the brain? How do they differ?
Hindbrain: reptilian brain taking care of basic physiology.
o Ex: Odin's curse where you lose ability to breathe automatically
o Partially controlled by higher limbic structures.
Midbrain: mamalian brain; limbic system; emotional brain
Forebrain: the cortex; our abstract associational level
o Bidirectional communication with the limbic system
The Papez circuit and its myriad effects on the hypothalamus. Know the structures, their basic
functions, and their connections!
Structures: Hypothalamus, amygdala, septum, hippocampus, mammilary bodies, thalamus, ventral tegmental
area (VTA), nucleus accumbens, frontal cortex.
Connections: amygdalo-fugal pathway, fimbria fornix, medial forebrain bundle, mammilo-thalamic tract, stria
terminalis, cortex-limbic connections
How does a structure go about having its strongest effect on the hypothalamus?
o Whatever has the fewest synapses between it and the hyp.
Why is the stria terminalis so weird?
o It's one LONG neuronal tract that loops around the hippocampus between the amygdala and the hyp.
o Reflects the movement of brain regions during embryonic development and because brain evolution is one
system duct-taped on top of another.
What are the subnuclei of the hypothalamus and what are their functions?
Ventromedial hypothalamus: female sexuality
Medial preoptic area: male sexuality
Suprachiasmatic nucleus: circadian rhythms
Paraventricular nucleus: makes CRH
Arcuate nucleus: location of release into the hyp-pit portal circulation
Lateral hypothalamus: hunger
How do we study the brain (and the limbic system specifically)?
Lesion studies like H.M.
Stimulating electrodes (or Transcranial Magnetic Stimulation, Steven's favorite!)
Recording electrodes (for electrical or chemical recording)
Gene expression and other molecular techniques (what NTs are at work?)
Imaging (anatomy)
o Structural plasticity seen in London taxi cab drivers' hippocampi. Amygdala larger
with PTSD.
What caveats do you have to watch out for when trying to infer brain function?
Centers vs. fibers of passage
Behavior doesn't lend itself well to a "center" concept: more distributed in reality
Ethological perspective is vital: what does the behavior mean for the survival of that animal?
Individual differences like rank can cause very different outcomes from stimulation: rank in baboons, for example,
influences how they respond to a threat yawn
What is subliminal presentation? What brain region responds to it?
Amygdala is easily activated by stimuli so subtle or quick that you don't consciously recognize them. It then
influences the hypothalamus which influences the body.
Explains anxiety triggers in panic attacks and PTSD that are too subtle to be consciously perceived.
How is CRH tied to alertness?
When something is different/novel/unexpected the hippocampus recognizes that and alerts the hypothalamus to
get CRH moving to stimulate alertness.
How do the hippocampus and amygdala mediate fear memories?

Amygdala tends to "remember" the specific, most salient fright cue
Hippocampus tends to "remember" the context, the surroundings
How is the limbic system regulated by the peripheral bodily physiology?
Called the James-Lange theory of emotion. The body tells the brain what to feel.
Peripheral physiology influences emotional state.
o Ex: (note from extended notes): administer epinephrine, lie to people about it, and they then interpret their
aroused physiology as intensifying whatever emotion was triggered by their social context.
o Ex: holding a pen in the mouth as a frown or a smile influences people's mood.
o Ex: benzodiazepines as muscle relaxants peripherally also decrease anxiety
o Ex: good posture makes you prouder
Example Exam Questions

1. In the triune (tri layer) brain concept, the ________________ is considered to comprise the third layer. From a
functional standpoint, one part of this region, called the ___________________ is considered by many to be
actually part of the ________________, which is considered to be part of the 2nd layer of the brain. (4 pts)
Why is that? (2pts)
2. The post synaptic neuron is repeatedly exposed to massive levels of neurotransmitter. Over time, what changes
might occur in receptors in the post-synaptic neuron? (1pt).
To call the study of chaos "nonlinear science" is like calling zoology "the study of nonelephant animals"
- Stanislaw Ulam in Chaos
Reductionism and Chaos

What are the historical origins of our modern reductionist science?
1. Dark Ages: a whole lot of tremendous knowledge was lost.
2. Somewhere along the way (Enlightenment), a lot was re-discovered and invented, like reductionist thinking.
What are the big ideas of reductionism?
a. You can break things down into component parts, understand the parts, and therefore understand the
complex whole.
b. Putting the component parts back together in a linear, additive manner will produce the complex whole.
c. Know the starting state, and you know the ending state. Further, a simple, small change in the starting
state leads to a simple, small change in the end state.
d. Complex reductive systems need plans/blueprints (and a master planner to make those blueprints).
e. Variability is just noise/signal error/instrument error. The ideal solution is out there; all you need is more
powerful tools to find it.
Of course, this reductionist view runs into issues in some areas of science. Like what?
1. Problem: insufficient numbers of component parts
a. Not enough neurons for a reductive brain based on simple dot/line/shape recognition building up to
grandmother neurons. Solutions?
i. Instead we see sparse coding in some neurons that respond to relatively few
complex stimuli (like Jennifer Anniston and the Sydney Opera House). Almost
like grandmother neurons. That's not the majority of cases though.
ii. Instead, we have networks of neurons (or different nodes in the networks)
representing many different things. (more to come on this below)
b. Not enough genes
i. For the bifurcations of the circulatory system, pulmonary system, or dendritic trees on neurons.
1. These systems bifurcate at the level of single dendrites, at the level of dozens of cells in a
capillary wall, at the level of thousands of cells in lung bronchi bifurcations.
2. But there just aren't enough genes for this style of genetic bifurcation!
c. You also can't have a purely reductive system of deterministic predictability when there is so much chance.
i. Ex: fish hierarchies do not follow predictions of the dyadic interactions.
ii. Ex: brownian motion in distributing mitochondria, TFs, other cytosolic things
when zygotes split and twin.
iii. Ex: random transposable genetic events during neurogenesis.
2. THE MOST FUNDAMENTAL FAILURE of reductionism: nonlinear chaos
a. What are the characteristics of nonlinear systems?
i. You can't predict the final state from the starting state. You have to go through every step.
ii. Divergence/butterfly effect: small changes in the starting state can produce
large changes in the ending state. A nonlinearity.
iii. Convergence: large changes in starting state can minimally affect the final state.
A nonlinearity.
iv. Scale free: starting states of 26 and 27 can have as much difference than
starting states of .00026 and .00027.
v. They ARE deterministic, just not predictable many generations into the future. Randomness and
chance (above) are what we mean by systems that would NOT be deterministic.
b. One way of summarizing all that: sensitive dependence on initial conditions/the butterfly effect.
i. Illustrated with cellular automata and their interactive reproduction rules.

ii. What are some key features of cellular automata, their rules, and their outcomes?
1. Most starting states go extinct
2. Most others create boring patterns (like all-filled-in). This is a "non-organic" analogy. Like the
structure of a rock or crystal.
3. Only a few interesting, dynamic mature patterns emerge as possibilities from very different
starting states. Thus you're likely to converge on those.
4. You can't predict generation thirty based on generation one. You have to go through all the
intervening generations.
5. Asymmetric starting states tend to produce dynamic, fluctuating mature states more than
symmetric starting states.
c. Translating these findings to the biological realm:
i. Vast majority of species have gone extinct.
ii. Biological systems converge. Ex: high-altitude plants and their convergent evolution.
1. Knowing the final (converged) state doesn't tell you about the starting state.
iii. The butterfly effect/divergence illustrated by macroevolutionary mutations (TFs, splicing enzymes)
iv. You get patterns in seashells that mimic those of the cellular automata handout from class!
3. Chaotic systems
a. Understanding "deterministic" and "periodic:"
i. Deterministic and periodic. Like a simple "add one" rule. 1, 2, 3, 4, 5
ii. Deterministic and aperiodic. You can't just repeat the same step over and over, the state changes
with every iteration. It also NEVER actually repeats a previous state or else it would be periodic. The
difference might be 10 orders of magnitude down the line, but the difference is there. This is what
we're usually talking about in chaos.
iii. Non-deterministic and aperiodic. This would be utter randomness, with each new generation not
even following any rules, but just generated at random. This ISN'T what we're talking about in class.
b. Ex: The water wheel
At some speed of water going in, you get aperiodic oscillations. They ARE deterministic, just NOT
predictable.
You can figure out what's going on at time T+1, but you can't extrapolate to T+10 without going
through T+1 then T+2 then T+3, etc.
c. Ex: Strange attractors
i. Attractor: The name you give to the "ideal
solution"
1. Perturb a non-chaotic system and the curve
will return (be attracted to) its original path.
2. Chaotic systems never achieve this. Perturb
them and you're just off on a different
chaotic path.
iii. There is no perfect idealized point that we're all
failing to achieve. There is no norm, no correct
answer. The variability, the fluctuation: that is the
norm.
4. Ex: Inherent variability and fractals
a. The variability never goes away, even as you zoom in with more
and more powerful tools. "The average" maybe doesn't actually
represent the true nature of the system. Maybe variability is
inherent.
b. "fractal" can be talked about in a number of ways/definitions.
i. Noun: "A pattern whose variability remains constant,
independent of scale."
1. Like the strange attractor
2. Like Sapolsky's testosterone meta-analysis

ii. Noun: "A pattern that is self-similar over a range of scales."
1. Like the Mandelbrot set:
2. Like bifurcating systems in the body
iii. Noun: "A pattern with complexity best described as being a fraction of a dimension."
1. Like the Koch snowflake, Cantor Set, or Menger Sponge
2. Sort of like the circulatory system: huge surface area and minimal volume.
iv. Adjective: describing any of the above patterns.
5. Reductionism isn't ALL bad though. Great for crude answers and explanations. Or for predicting things 99% of
the time. Reductionism can be great on the average. But itll rarely give you a 100% clean, predictive system.
Emergence and Complexity

1. Context: instead of "you can't predict anything complicated, you can't understand it, you can't manipulate
anything to control complex outcomes" consider all that is to follow. It's about a type of "predictive" power
pretty different from things you've probably considered before.
How do we solve the problems of insufficient numbers of component parts?
1. Neural networks instead of grandmother neurons.
a. Patterns of neural activation in overlapping networks can code for concepts, ideas, etc.
b. "The key point is that networks not only overlap, but that there are foci of convergence and foci of
divergence one thing can have a lot of connotations, while you can be prompted to recall something by a
lot of different things."
2. Fractal patterns in bifurcating systems instead of a different gene for every bifurcation.
a. The bifurcations are fractals in that they are self-similar over a range of scales.
b. Thus the rules that govern them could be fractals, thus, hypothetical fractal genes that somehow encode
for rules like "grow 5x the diameter of the tube, then bifurcate" which repeat over and over across many
systems.
c. They could code for adhesion proteins between cells that become unstable after it's grown a certain length.
d. You can then have fractal mutations. We see things that look like this, but it's obviously not a perfect
explanation with solid evidence yet, but a decent theory for now.
e. Good evidence for something like fractal genes going on:
i. Some genes are relevant to both vascular bifurcation and lymphatic bifurcation, as a side example.
ii. Fractal mutations give something called Kallman's syndrome where bilaterally symmetric structures
that form around the midline of the body's axis have developmental problems.
f. These fractal patterns help solve problems of "not enough space" for the circulatory system
i. Every cell is 5 cells away from a blood vessel. So blood vessels have HUGE SURFACE AREA.
ii. But the circulatory system takes up less than 5% of the body's volume. So TINY VOLUME.
iii. Sounds just like?
1. Menger sponge! Fractal geometry for the win.
What are our examples of crude "pre-emergence"?
1. Potato chips have an emergent double-saddle shape by virtue of biophysical features of the system.
2. Wisdom of the crowd.
a. Unrelated to average IQ or expertise of the individuals.
b. Related to how well they communicate, and giving weights to more expert sub-group helps.
c. Does worse if:
i. Very strong and extreme positions
ii. Shared biases
iii. Zero expertise
iv. You know what other people are inputting
d. Not "true" emergence because there's no interaction among the elements.
What are the components of true emergence? Very important.

1. No plan, no blueprint, no mastermind.
2. Many parts interacting. Many parts behave fundamentally differently from fewer parts.
3. Simple rules.
4. Random encounters.
And examples of true emergence?
1. (emergence: complex systems/patterns arising out of a multiplicity of simple interactions)
a.
2. Ants
a. They self-organize, an emergent property that arises when you have enough
constituent parts interacting according to certain rules. (works for marching bands
too). But you need enough parts.
3. Swarm intelligence
a. Connecting the nodes with two generations of ants (or bees or any other component with one generation
following another).
b. The better the quality, the more intense the signal left my generation 1 for generation 2. That's the rule that
allows these systems to work.
c. Can solve the traveling salesman problem optimally.
d. Works for the wiring of the cortex. First generation: radial glia. Second generation: neurons.
4. Combinations of attraction and repulsion forces
a. Works for urban layouts
b. Works for neuronal development, producing distinct nuclei and fibers of passage.
c. Works for the origin of life with things like amino acids emerging from simple atoms and molecules.
5. Power law relationships in the connections of networks. What does this mean? What are some examples?
a. Many connections to nearby nodes, fewer connections to very distant nodes. 20% of the neurons will have
80% of the connections Like 80% very local and 20% longer-than-local (with a very long tail: very few super-
long connections).
i. Works for phone calls, emails, website links. earthquake intensities.
ii. More interestingly, works for neuronal networks.
iii. Autism as involving many short-distance connections at the expense of long-
distance connections.
6. Bottom-up quality control
a. Amazon.com recommendation
i. You write reviews.
ii. Good reviews are rated/weighted in terms of quality
iii. Those who wrote the 'good reviews' have more judgment power over other reviewers
iv. Thus emergent, bottom-up quality
b. What are the drawbacks to bottom up quality control?
i. Early on it's pretty haphazard before true quality control emerges
ii. Assumes people who write good reviews are also good judges of reviews. Not necessarily true
iii. Can produce tremendous conformity. Everybody's told to try other similar things instead of
something truly unique and potentially interesting.
How does emergence apply to humans?

1. Our 2% of genetic difference from chimps: ~1% is olfactory differences, body hair, immune function,
reproduction. The OTHER ~1% are things like TFs that amplify differences in things like neuronal cell divisions.
a. We have the same neurons as any other animal
b. We just have a lot more of them and thus more capacity for emergent properties.
Summary of chaos/complexity/emergence themes:
More is different.
The simpler the iterative components, the better.
Encourage random encounters.
Look for gradients of information.
Pay attention to neighbors.
Generalists are more valuable then specialists.
There are no idealized norms.
Complex, adaptive systems occur without blueprints
Example Exam Questions for chaos/complexity:
1. What is a fractal? (2 pts)
2. What could the rule be for a fractal gene encoding bifurcations in a system? (2 pts)
3. What might be the effect of a fractal mutation? (2 pts)
4. In no more than two sentences, give a real-world example of convergence: (2 pts)
5. In a fully-developed brain, what structural component is described by a Power Law? (2
6. A number of examples in class were presented in which chance plays a large role in a seemingly deterministic
process. List two: (2 pts)
7. Give an example of a system that is based on the attraction/repulsion rules of cellular automata: (1 pt)
8. Give an example of a human invention that has been generated with a bottom-up approach: (1 pt)
9. If two identical dynamic systems have almost-identical starting states, then their ending states will be similar
(circle one) (2 pt)
TRUE FALSE
10. If two identical dynamic systems have almost-identical final states, then their starting states must have been
similar (circle one) (2 pt)
TRUE FALSE
11. Give two examples of bifurcating systems: (2 pts)
Sexual Behavior (lecture 1 of 2)
Things to know for sexual behaviors

How sexual behavior must be very similar, but not identical across species.
A few features of human sexual behavior that may or may not be uniquely human.
Some brain regions that are relevant to sexual behavior that are unique to one gender, and ones common to
both.
Dopamine as fueling goal-directed behavior; vasopressin interactions with dopamine systems and social bonding.
Some examples of pheromone effects on reproductive physiology and behavior within gender and between
gender; evidence regarding humans.
The effects of menstrual cyclicity on sexual behavior and motivation in various species, including humans.
What testosterone has to do with promoting sexual behavior.
Development not refining the features of the FAPs of sexual behavior but, instead, teaching appropriate social
context.
Why the neurobiology of testicular feminized males supports a strong role of environment in causing sexual
identification.
Some features of inter-sexual competition in the realm of reproduction.
Some alternative strategies to male-male competition exploited by males in various species.
Some of the theorizing about the evolution of homosexuality.
Attractiveness: the roles of symmetry, conspicuous markers of health and fertility.
How to make sense of homogamy in an evolutionary context.
What do sexual behaviors look like?
FAPs: orgasm, lordosis, pelvic thrusts, erections
FAPs serve as releasing stimuli for other FAPs and back and forth
Have to interview in animal's own language! Ethological examination of sexual behavior is key.
Why do animals do it?
Because it feels good! Primacy of sensation.
Why are FAPs so conserved similar among species?
Do it differently and you probably won't have any offspring.
But what argument runs counter to that idea?
Species do need to do it in their own way. Don't want to waste time mating with other species.
Know the basic vocab
Libido; attractivity v. proceptivity v. receptivity; motivation v. performance (ex. erectile dysfunction); desire v.
arousal v. orgasm.
How do you do the randomized reporting to learn about "taboo" sexual behaviors?
Example from the '80's of whether a man had slept with another man.
You're the man responding:

o If yes, just mark yes.
o If no, flip a coin. Heads you mark yes (so you marked "the taboo answer" just due to the coin flip, not actual
behavior). Tails you mark no.
Now you're the researcher
o Take the number of "nos" you got and double it. That's the real number of no's. The rest are real "yeses"
o For example: in actuality, 10% of the men had slept with another man.
Those 10% mark yes.
The other 90% have not, but 45% will mark no and 45% will mark yes.
So your responses will come in: 55% yes, 45% no.
You know that the "nos" are only half what they should be, so you know it's actually 90%no and 10%
yes.
Why do females have orgasms? Some theories:
Sperm facilitation (increased vaginal fluid)
Post-coital exhaustion and sperm motility
Reinforcement quality no evidence of higher fertility in orgasm-prone women though
Some twin evidence for genetic influence, with caveats
Spandrel: necessary for males so same physiology in females. Parallel of nipples in men.
What are four intercourse-related male-male competitive strategies?
Copulatory locks
Sperm plugs
Spiders cementing other spiders' genitals
Other insects insert their own sperm into testes of other males (fun fact!)
For human sexual behavior, what behaviors were once thought to be unique but now not so
much?
Things that once were unique, but now are not: nonreproductive sex, foreplay, variety, homosexuality, rape,
masturbation, fantasy, foreplay
And what actually does seem to be unique?
Sex in private, egalitarian sex, marriage (and cheating), romantic love, the expectation of sustained romantic love
o Ex. Divorce period = 2-4 years humans are serial monogamous (move from one monogamous
relationship to another with inter-birth interval)
Compared to other species, were kinda boring. Other species have hermaphroditism, sequential
hermaphroditism, pseudohermaphroditism, parthenogenisis
What is the neuroscience of sex?
How do the sexes differ in the functions of various sex-related brain regions?
Females:
o Ventromedial hypothalamus - high levels of receptors for estrogen and progesterone, essential for female
reproduction
o Midbrain structures: Relays from hypothalamus to the autonomic nervous system in the spine ex.
Lordosis reflex
Males:
o Medial pre-optic hypothalamus: sexual performance, testosterone receptors
o Amygdala: sexual motivation (and aggression)
And what are universal neurobiological aspects of sex?
Autonomic nervous system used for erections in both sexes animals can have vascular or muscular.
Orgasm is a shift from parasympathetic to sympathetic nervous stimulation. After orgasm, females on average
take longer to return to physiologic baseline than males.
(side note) how does the dopamine system work?
o Something to do with pleasure, reward, anticipation, motivation.
o Active especially in ventral tegmentum and nucleus accumbens (the mesolimbic dopamine circuit)
o Spontaneous reward activates dopamine system.
o But on closer study it's also true that dopamine is about anticipation of a reward and fueling the goal-
directed behavior to get the reward.
o Highest dopamine response (fueling reward-seeking behavior) in the context of intermittent rewards:
maybe.
What does dopamine have to do with sex?
o Attractive pictures of women activate these regions in heterosexual men. More attracitve --> more
dopamine.
o D1/D2 dopamine receptor situation
Receptor location
D2 receptors are on the post-synaptic neuron per usual
D1 receptors are pre-synaptic autoreceptors, the bookkeepers.
Receptor function
D2 stimulation facilitates formation of a new pair bond
D1 stimulation does the opposite: makes voles uninterested in forming
pair bonds
Plasticity
D2 receptors up-regulated in the dopamine circuit when voles are first
mating. Forms the pair bond.
After pair bonding, D1 receptors are up-regulated, so they aren't inclined
to form new pair-bonds
What region is associated with long-term relationships and feelings of comfort, familiarity, needing?
o The anterior cingulate
What's the role of the frontal cortex in sexual behavior? What NT does it tend to use?
o Tends to use serotonin, but receives lots of dopamine projections.
o Makes "the hard choice."
Could be inhibiting sexual impulses in inappropriate contexts.
Or could be fueling sexual impulses in cases where it's scary/difficult to do so.
What are the endocrine RESPONSES to sex?
How do hormones differ between genders in RESPONSE to sex?
Females:
o Progesterone increase (reinforces pleasure, prepares for pregnancy)
o Androgens increase (mediates sexual motivation)
o Oxytocin increase (attachment, trust, mediate release of dopamine for pair bonds)
Males
o Testosterone increase AFTER sex
o Vasopressin increase we see high levels of vasopressin receptors in meso-limbic dopamine system of
pair-bonding species, which cause dopamine release (increasing monogamous behavior)
Ex. Change VP receptors in voles can cause poly to be mono
Ex. Men with mono version more likely to marry and not divorce
Remember: this is the vasopressin receptor promoter that has the variation, not the receptor itself.
So it's about expression patterns.
Take-home point (THP): express vasopressin receptors in the mesolimbic regions of the brain and the
animal will be more likely to be monogamous.
What's the neurobiology of sexual orientation in males?
The INAH-3 (interstitial nucleus of the anterior hypothalamus) comes in different sizes.
o Men have a 2x larger INAH-3 on average with huge variability and overlap compared to women.
o One finding from Simon LeVay shows that gay men's INAH-3 is about halfway between the size of straight
men and women. Has confounds because the gay men had died of AIDS.
Finger-length ratios and otoacoustic emission also show a gender difference with gay men, on average, between
straight men and women.
And the nbio of sexual orientation in females?
o "The literature here is smaller than for male sexual orientation. Some studies suggested elevated levels of
androgenic hormones in lesbians versus straight women, some suggestions of elevated prenatal exposure to
androgens. A few studies suggest that the 4th to 2nd finger ratio in lesbians differs from that of straight woman,
in the direction more of the male average. Ditto for otoacoustic emission. Theres also some studies suggesting
male-like cognitive profiles in terms of visuospatial tasks, verbal fluency. Of note, though, these are all very
small effects, highly variable. A few studies have suggested that these patterns are more pronounced in lesbians
who are self-described butches (i.e., women who take more stereotypically masculine roles during sex)." -from
Extended Notes
And the nbio of transsexuality?
o Note on defining gender/sex: can be done by chromosomes, gonads, hormones, external genitalia, secondary
sexual characteristics, and/or psychosocial identity.
o The BNST (bed nucleus of the stria terminalis) comes in different sizes.
o Large sex difference in the size of a part of the BNST with a lot of predictive power
o In transgender people (who feel their anatomical sex doesn't match their identity), the BNST tends to be
the size of the sex they feel they should be rather than the one they are.
o Conclusion: maybe less of a "psychological pathology" as it's been thought of; more a case of being stuck in
the body of the wrong gender.
o "Around 60% of men who have had their penises removed (because of penile cancer) have phantom penis
sensations, whereas male-to-female transgendered individuals do not." -Extended notes
The Releasing Stimuli for Sex
What examples of visual releasing stimuli do we have?
o Rhesus monkeys pay for sexual imagery of female rhesus monkeys (esp the perineum of a female in estrus). Also
pay to see a dominant male - might be "gathering information."
o Both sexes in humans have the amygdala, hypothalamus, and mesolimbic dopamine systems activated when
viewing a picture of somebody they find sexually attractive.
Tactile stimuli?
o Lordosis!
o Also skin can be more sensitive if and only if you have certain levels of gonadal hormones.
o Touch evokes activation of dopamine systems
Olfactory stimuli?
o Pheromones! They're breakdown products of sex hormones. What can you know by smelling them?
o Gender, age, fertility, reproductive state
o What do you need to detect them?
o Intact gonads
o What are the intrasexual effects of pheromones?
Gustatory stimuli?
o Some ungulates do flehmening where they lick each other's genitals to gain the pheromonoal information.
Auditory stimuli
o A stag's roar can induce ovulation in females.
o Pandas and human females have slightly higher pitched voices around ovulation
OTHER stimuli?
o Thought: like fantasy in humans (and Sapolsky would say in his baboon observation)
o Rage/fear/stress: inhibit sexual behavior and physiology
o Variety and the Coolidge effect. A new partner can re-invigorate sexual motivation. More often
found in males than in females.
Sexual Behavior (lecture 2 of 2)
How Hormones in Adulthood Affect

Sexual Behavior
First: note what we mean by "sexual
behavior."
Proceptive, receptive, attractive behavior.
Erections, pelvic thrusts, lordosis, likelihood of
orgasm, interest in sex, etc.
Second: note what we mean by
organizational vs. activational effects
Organizational: perinatal environmental
hormones. Setting up the framework and the
structuring for the whole life.
Activational: acute hormonal effects in adulthood. Immediate triggers.
Where in the menstrual cycle does sexual behavior peak in most female animals? In humans?
Most animals: peaks at ovulation. Sometimes only occurs at ovulation.
Humans: same thing, but also get a peak at menstruation, hypothesized to be due to "relief" at
not having gotten pregnant.
What effects are female hormones having?
Estrogen works in brain to increase progesterone and oxytocin receptors in the limbic system.
Skin more sensitive to touch
Androgens also present (at 5% the level of males), involved in sexual motivation.
What does Testosterone (T) have to do with male sexual behavior? How do we know?
Castration (no T) reduces sexual behavior, but it doesn't go down to 0. Replacing T at 10%,
100%, or even 200% the original levels causes sexual behavior to come back at the same level.
Only with 1000% T way above normal physiological levels do we get an increase in sexual
behavior.
When castrated, animals exhibit amounts of sexual behavior proportional to their pre-castration levels showing
that sexual behavior is also determined by the environment and experience, not just T.
It doesn't initiate neuronal action, testosterone potentiates the effects of other excitatory stimuli.
How do we go about having seasonal matings? Why would we?
How: use melatonin. A hormone whose release is inhibited by light exposure. When day lengths are increasing,
you're approaching summer; when decreasing (one day compared to the next), you're approaching winter.
Why: want to give birth during fertile spring/summer times when offspring can survive best.
Who: depends on gestation period. If 2 month gestation period then melatonin stimulates reproduction (you have
a lot of melatonin in the winter, just before spring birth). If 6 month gestation period then melatonin inhibits
reproduction.
How Early Environment Affects Sexual Behavior

What happens to socially isolated primates' sexual behavior?
Can still do it, just don't know the right contexts.
What social imprinting happens in human children?
You learn who the appropriate targets for sexual behavior are.
Kibbutz studies show us that's how we "learn" who our siblings are.
What role does early environment play in the development of homosexuality?
No evidence that it has any role. "neurotic homosexuality" caused by mothers and "absent father" theories
haven't held up to scientific scrutiny.
How Perinatal Hormones Affect Sexual Behavior
What is a "feminized" brain vs. "masculinized" brain? How accurate is this dichotomy?
Feminized: Hypothalamic gonadal hormone signaling is cyclic (ovulation, menstruation, etc)
Masculinized: produces male reproductive FAPs like erections and pelvic thrusts
Tons of animals fall in-between. An artificial dichotomy.
Through what pathways does T have its effects?
Peripheral body effects: converted to DHT and influences sensation.
Few areas of the brain: acts just as T, no conversion.
Most areas of the brain: is converted to estrogen and binds to estrogen receptors.
How do females avoid a masculinized brain?
They would have one because of all the estrogen floating around their prenatal environment
But estrogen is pulled out of fetal circulation by alpha-feto protein
In what cases are females "masculinized." And what are their outcomes?
Two ways:
o DES drug exposure generates high androgen levels during pregnancy
o Congenital adrenal hyperplasia
Outcomes:
o Less interest in "female-typical" sexual behavior and roles. More likely to be gay.
Confounds: many reconstructive genital surgeries and being a taller, more muscular woman
What is the case of testicular feminized males? How do their bodies and brains develop?
Born XY (genetically male) but androgen receptor mutates. T doesn't have bodily effects (as DHT).
But in brain T is converted to estrogen and thus produces a masculinized brain.
Male secondary sexual characteristics emerge at pubertyGender identity and bodily characteristics usually remain
female.
Do gay men have "feminized" brains? Why yes? Why no?
Yes: more older brothers increases likelihood of being gay because mother has antibodies that target T. Less T on
board, therefore a "demasculinized" brain.
Probably no: gay men have a lot more sex (look more "masculinized" than straight men in that respect).
Genetic influences on Sexual Behavior

How do you interpret the twin study research on sexual orientation?
Full siblings are only 9% concordant for sexual orientation, so the higher percentages in DZ and MZ twins are
probably due to environment (esp fetal environment!).
And the Hammer studies showing genetic markers?
o Not the same marker in different pairs
o Not replicated
o Poor scientific reputation
Evolutionary Influences on Sexual Behavior

Is sex for the purpose of social cohesion and cooperation?
Probably not. Probably more about reproduction.
Bonobos as exception.
Sex differences in promiscuity
Sperm cost a lot less than pregnancies so females are choosy and males are promiscuous. Most seen in
tournament species. Less seen in pair bonding species.
Males often try to control female reproduction across the animal and human kingdom. In what ways?
o Clitorectomies and chastity belts in nomadic societies

o Males actively decreasing the attractiveness of females to other males.
o Sperm compete with sperm from other males.
o Male domination and linear access models (with exceptions below)
o Also rape
o Also subterfuge
What female counterstrategies exist?
o Concealed ovulation to trick males
o Pseudo-estrus to trick males (esp in cases of competitive infanticide)
o Female choice. Sneaky sex in the bushes to subvert the linear access model: stolen copulations. They like
the nice guys (nice guys FTW!).
o Sperm dumping from males they don't prefer
How do we explain the evolution of homosexuality?
(this is assuming there are genetic influences: see above for why there's probably very few)
Heterozygote vigor argument
Traits that are maladaptive in males but adaptive in females
Kin selection: helper at the nest hypothesis. Evidence supports this hypothesis.
What traits are markers of a good mate?
Lots of support for symmetry.
o Women judged to be more symetrical when ovulating.
o Babies prefer symmetrical faces.
o A marker of health.
Secondary sexual characteristics like lions' manes, big bushy beards, colorful bird spots, etc. Why would these be
good markers for a mate?
o Handicap principle: I can be wasteful on these traits so I'm very fit. Lots of evidence here.
The worse the health and life expectancy in a country, the more women prefer faces
of men with pronounced secondary sexual characteristics! Interesting, no?
o Could be markers of immune competence. Esp with caretinoids in birds.
But males will try to cheat and put their last dying gasp of energy into their secondary
sexual characteristics so they can mate before they die.
o Markers of fertility.
Females: Like estrus swellings which indicate estrogen levels, earlier puberty, better
child survival.
Females: Like high breast:waist and low waist:hip ratios indicating fertility.
Males: Like jutting jaws, high foreheads, heavy musculature indicating high T.
But how do these markers run into the problem of a self-fulfilling prophesy?
o Take a given male bird and the females don't like him that much. But then surround him with fake female
birds: make him seem all popular. Then all the other females now like him. A bandwagon effect.
Interpretation: other females recognize that this male can attract females, so offspring of this male
will be able to attract females and thus have high fitness. Therefore those females will have high
fitness. Has individual selection written all over it.
What features of human couples show a lot of homogamy?
o
Religion, age, race, ethnicity, politics, SES Shared in 90% of couples
IQ, education, introversion/extroversion >40%
Height, weight, hair color, eye color, width of nose, length of earlobe, lung <40% but still significant!
volume
What did the Buss study find as to what people really want in a mate?
o Women more likely than men to value financial status in a mate
o Men more likely than women to value youthfulness, fidelity, and fertility.
o OVERALL EVERYBODY JUST WANTS SOMEBODY KIND AND INTELLIGENT. Yay humanity.

14) Cite two traits suggesting that Homo sapiens have not evolved as a classic pair-bonding species. (2 pts)
15) a. A pathway is now understood explaining how a male vole from a species that pair-bonds becomes
monogamously attached to a female. When he first has sex with her, he secretes the neurotransmitter/
neuromodulator ______________, which binds to its receptors in a brain region called _______________.
This excites those neurons to release ___________. (3 pts total)
b. What happens to a male vole in a polygamous species if you engineer neurons in that part of the brain to
overexpress the gene for the receptor for that hormone? (2 pts)
______________________________________________________________________
c. The increase in receptor levels engineered in part b was performed in a way that kept the amino-acid-coding
sequence of the protein completely unchanged from that of normal voles. What stretch of DNA was changed to
increase levels of the receptor protein being made? (1 pt)
_______________________________________________________________________
d. You find out that your brother John has a mutation resulting in significantly decreased expression levels of
that receptor protein. What can you conclude about the number of wives John will have in his lifetime? Justify
your answer. (2 pts)
__________________________________________________________________________________________
______________________________________________________
b. Pre-natal masculinization of a rodent brain results in (circle one for each) (4 pts total, 1 pt each)
1. a thinner corpus collosum
TRUE FALSE
2. cyclic GnRH release
TRUE FALSE
3. fewer hippocampal neurons
TRUE FALSE
4. a smaller sexually dimorphic nucleus (SDN)/INAH
TRUE FALSE
Aggression I
Big themes here:
Aggression itself isn't good or bad. It's all about the context in which it is expressed.
Human aggression and empathy is both remarkably similar to animal precedents, and also remarkably unique in
some cases.
The frontal cortex is all about doing the right but hard thing. It's also important for controlling behavior (NOT
about knowing what's right and wrong).
What aggressive behaviors look like

What human aggressive behaviors also have animal precedents? How about anti-aggressive
behaviors?
Aggressive: Murder, weapon use, organized violence, genocide, rape
Anti-Aggressive: reconciliation after fights (in bonobos, most likely to be sexy reconciliation time), empathy,
justice, cooperation (remember reciprocal altruism?), dominance hierarchies reduce aggression when stable and
working well, even bottom-up egalitarian hierarchies.
What behaviors in general are hard to classify as aggression or not?
Patas monkeys never fight in the wild. Their whole social structure keeps males away from each other and there's
no aggression. But bring them together they're insanely violent. So does this count as an aggressive or not
aggressive species?
Play fighting.
Hunting and predation.
What human aggressive and anti-aggressive behaviors DON'T have good animal precedents
Aggressive:
o Aggression displaced over space and time
o Passive aggression
o Bizarre Indonesia village murder raids bringing along an orchestra "to make it more
beautiful."
Anti-aggressive
o Charity displaced over space and time
o Reconciliation and forgiveness to talk it out afterwards
o Purposely forgiving and loving the most reviled people in society: nun Helen Prejean.
Neuroanatomy of aggression (seconds before the aggressive behavior)

What's our main "aggressive" brain structure? What else does it do? What's the evidence?
The amygdala!
Also does: fear and anxiety, male sexual motivation, emotional memories
Evidence: from lesions, stimulation, recording: all our traditional methods.
o Those with amygdalectomies don't understand angry faces, won't defect against cheaters, a lot less violent.
Note: they tend not to look at the eyes of scary faces. Interpretation: they're less sensitized to
aggressive releasing stimuli in the world.
o Scary images activate the amygdala.
o Epileptic foci near the amygdala bring aggressive thoughts just before seizure.
o Charles Whitman, famous mass murderer, had inexplicable aggressive thoughts leading up to the event, also
had amygdala tumor.
o Amygdalae in those with social phobia activate in response to faces
o Amygdalae in those with major depressive disorder activate in response to sad faces
Frontal cortex
How do frontal cortex neurons help you do the harder but right instead of easier but wrong decision?
o They modulate and potentiate other neurons to fire at lower thresholds. Not so much about direct
activation.
o They use dopamine to fuel goal-directed behavior to get the reward
What is executive function? How is it shown?
o It's the keeping in mind of rules. It allows you to override your impulses.
o It "chunks" the list of grocery items into logical categories
o Postpones gratification.
How does the legal system treat culpability in the context of knowing right/wrong, doing the right/wrong thing,
and the frontal cortex?
o You can know right from wrong, but with frontal cortex damage, you can't make the right
choice.
o Shown by the M&Ms study. Reach for 1, get 5. Reach for 5, get 1. With frontal damage you
can't help but reach for 5.
o The M'Naghten Rule: you're not culpable if you can't tell right from wrong. But those with
frontal cortex damage can tell right from wrong, but have instead a organic involution.
Can't engage the right action.
But how is this "frontal cortex loss = aggression" story complicate? What various forms can frontal disinhibition
take?
o Some people with frontal cortex are just really "aggressive" chess players or are disinhibited when it comes
to telling knock-knock jokes.
o Old people lose frontal cortex neurons and sometimes they're just inappropriately critical.
What is repressive personality and what frontal cortex patterns is associated with it?
o Highly disciplined and regulated. Not depressed or anxious. Tend to be successful.
o Elevated stress hormone levels even when not stressed. Frontal cortex has hypermetabolism even at
baseline.
Compare that to sociopaths
o Aggression without remorse and without feeling
o Hypometabolism (lower basal activity) with frontal cortex, elevated frontal cortex activity in the context of a
self-control task. Interpretation: they have to work a lot harder to pull of the same regulation that
everybody else does.
How do the amygdala and frontal cortex interact?
Bidirectional projections
You need a frontal cortex on board to get fear extinction
What is the lateral hypothalamus all about in the context of aggression?
Used to think it was a major aggressive center. Stimulate it and rats attack and kill mice.
But it's actually just hunger and that's predatory behavior
How is empathy mapped out, neuroanatomically?
The anterior cingulate activates both when YOU and a LOVED ONE are poked with a pin.
There's also a lot of hype about mirror neurons in the motor cortex but without much substance behind the
theory.
How is disgust/moral disgust mapped out neuroanatomically?
The insular cortex is active in humans for gustatory AND moral disgust.
It does this abstraction, this symbolic cognition based on bodily systems.
Where else do we see this abstraction/concrete cognitive interface play out?
Holding warm drinks makes you evaluate people as nicer, "warmer"
Sitting in a hard chair makes you judge others as meaner, more "hard-assed"
Primed to think of the country as a person and then read about bacterial invasions and people
are less sympathetic towards immigrants.
Washing your hands after sharing your moral failings makes you less likely to help people.
All this showing that evolution is a tinkerer, not an inventor. Duct-taping metaphors onto concrete brain
functions.
How does the anterior cingulate influence pain/depression?
Substance P is the NT involved. Block substance P signaling and you block pain, but it also works as an
antidepressant. Interpretation: depression is in some way about psychic pain.
How does the brain react to the trolly problem? How about when the judge instructs a jury?
The frontal cortex decides to pull the lever
The limbic system decides to not push the person
Judge: "we all have feelings for those with horrible luck in life but remember your job is to simply decide whether
or not a law was broken. Ignore your feelings." condition 1.
Activates frontal cortex
Judge: "laws are great, but it's about protecting the weak from the mighty." condition 2.
Activates limbic structures
Finally, what do the hypothalamus, midbrain, and brainstem regions have to do with aggression?
Highly active during aggression.
But it turns out that's just for any general state of arousal. Including orgasm etc.
(Same story with arousal hormones: epinephrine). Opposite of love is not hate; opposite of love is indifference.
Aggression II
Neurochemistry of aggression (seconds before the aggressive behavior)
What is the driving force giving your frontal cortex the power to do the harder but right thing?
Dopamine
Serotonin time
What are low levels of serotonin associated with?
Impulsive behavior. Impulsive aggression.
How does serotonin synthesis inform our understanding of its role in aggression?
Serotonin is made from tryptophan. The enzyme that does this conversion is TH.
When serotonin acts in a synapse, it is then either reuptaken or degraded by MAOb, an enzyme.
So these actually contradict the "serotonin = impulsive aggression" story. How so?
Poor MAOb variant means more serotonin will act in the synapse. But people with this variant have
more antisocial behavior.
And if TH works better you should have more serotonin. But people with better TH tend to have more
impulsive violence.
So it's complicated, m'kay?
Where else do MAOb variants come in?
The New Zealand kids study.
The "good" version makes you less vulnerable to developing antisocial behavior.
The "bad" version (less effective at degrading serotonin, leaving more in the synapse) predicts more
antisocial behavior. With more aggressive childhoods, more antisocial behavior. Need childhood
abuse to make it happen. It's a vulnerability. Gene-environment interaction.
What effect does alcohol have on aggression?
Same story that comes up over and over: it exacerbates pre-existing tendencies. Makes unaggressive individuals
less aggressive. Makes aggressive individuals more aggressive.
Also see this play out with cultures newly introduced to alcohol. They adopt the drunken behavior of the drunken
role models of their colonial occupiers.
What are the two profiles of alcoholism?
Profile 1: Increases risk of antisocial behavior. Drinking socially. Men.
Reaching age 30 and you're cured.
Profile 2: no gender difference. Alcoholism most severe in late middle age. Barely functioning alcoholics
drinking alone.
Heritability separates out the two lines.
Acute environmental triggers of aggression: Releasing Stimuli

What are some primate releasing stimuli for aggression?
Stress, pain, and frustration.
Taking out aggression on those under you works out great for baboons' stress levels. Might explain something
about your future boss
Ex: rape seen in baboons in cases of displaced aggression after alpha male jerks are dumped off their thrones.
Does crowding cause aggression?
Hormones in adulthood influencing aggression

What does testosterone have to do with aggression?
SAME story as with T and sexual behavior
So elevated T within normal physiological ranges does not cause increased aggressive behavior.
Could you say T causes aggression?
No! It's about modulating aggression. Add T to the amygdala (and do nothing else) and it
doesn't fire more, but when it is stimulated from some other structure, far more likely to fire.
What is the challenge hypothesis for aggression?
T generates aggression when resources are being challenged.
But it also generates pro-social behavior if being pro-social is what it takes to defend resources.
More cooperation in the ultimatum game where you have to be prosocial to win money (a resource).
Who is our big exception to typical sex patterns in T and aggression? What are the patterns in this
exception?
Spotted hyenas.
Females have more androgens, have clitorises like penises, fat pads like scrotums.
Their social system has females on top. They also give birth to only 2 cubs. What do you predict for their feeding
order?
Now cubs go first, then females, then males.
Opposite of how it is in lions.
How do we explain PMS?
Some hypotheses about it being a myth, invented by the west, a "dependent" personality style, a conflict between
being productive and reproductive etc.
Bleh to all that. Baboons have the same profile of irritability/aggression so it's probably biological. AND males
have the same mood shifts along with female partners' periods so it can't just be the hormones.
So it's biology within a social context.
It might also be about depression. How could you explain that with hormones?
Drop in progesterone near the end of the cycle.
Progesterone potentiates GABA, as you should recall.
Opioid levels also drop around the period.
Long-term environmental effects on aggression

How does Lorenz' hydraulic model of aggression hold up to scrutiny?
It would say aggression is inevitable, and should be less likely after previous aggression.
But aggression is NOT inevitable. And aggression tends to beget more aggression.
How about the frustration-aggression Marxist hypothesis?
Holds up well. A lot like displacement theories.
Exception: aggression goes down during periods of famine, of scarcity. This would argue that
aggression is more behavioral fat.
How about behaviorist accounts of aggression?
This would predict it's all about reinforcers: rewards and punishments. That will determine
aggression.
Sort of true: premeditated crimes are influenced by penalties. But crimes of passion are not.
Human infants develop ego boundaries, theory of mind, self/other distinctions.
These as precursors for empathy and pro-social behavior.
Necessary but not sufficient, as seen with sociopaths who have great theory of mind
Does violent TV make kids more aggressive?
How do you respond to the claim that violence is biologically predetermined, since aggressive
violence peaks in adolescent males?
You'd bring up the data comparing murder rates in Chicago/Toronto/London.
They all follow the same rates of violence curves.
But the absolute amount of violence is hugely culturally determined.
Take-Home Point: your long-term environment teaches you the social contexts that are appropriate for violence.
Huge predictor of violence: living in a culture that rationalizes violence

How does the pattern of amygdala activation change in persons suffering from major depression? (2 pt)
________________________________________________________________________
a. According to what you learned in Bio150 about aggression, which of the following could be an explanation
for increased aggression (circle all that apply, 5 pts total, 0.5 pt for each):
a) Tumor in amygdala
b) Lesion in amygdala
c) Lesion in INAH3
d) Increased basal metabolic activity in frontal cortex
e) Lesion in septum
f) Enlarged anterior commissure
g) Stroke damage to frontal cortex
h) Increased dopamine release in nucleus accumbens
i) Decreased sensitivity of testosterone receptors in amygdala
j) Increased basal metabolic activity in anterior cingulate
b. You conduct the appropriate tests for the explanations given above, but fail to find anything wrong with the
brain structure, brain chemistry, or endocrine parameters in this patient. You decide that he could have a pre-
existing genetic tendency and that perhaps a modulatory environmental effect could have increased his
aggression.
Which of the following are environmental factors that could increase aggression by having a modulatory effect
on a pre-existing genetic tendency (circle all that apply, 0.5 pts each, 3 pts total):
a) Living in a rural area

b) Being an alpha male and having just lost a fight to the #2 male
c) Having a particular version of the MAO enzyme
d) Drinking large quantities of alcohol
e) Increased sensitivity of testosterone receptors in amygdala
f) Being subjected to child abuse
c. After more extensive physical and psychological tests and background checks, you conclude that this patient
is 100% fine. No pre-existing genetic tendencies towards aggression, no environmental factors, no biological
basis. Despite killing 34 people, no criminal charges are pressed against him. Given what you learned about
aggression in class, why might the man have killed 34 people? (1 pt)
Aggression II
Neurochemistry of aggression (seconds before the aggressive behavior)
What is the driving force giving your frontal cortex the power to do the harder but right thing?
Dopamine
Serotonin time
What are low levels of serotonin associated with?
Impulsive behavior. Impulsive aggression.
How does serotonin synthesis inform our understanding of its role in aggression?
Serotonin is made from tryptophan. The enzyme that does this conversion is TH.
When serotonin acts in a synapse, it is then either reuptaken or degraded by MAOb, an enzyme.
So these actually contradict the "serotonin = impulsive aggression" story. How so?
Poor MAOb variant means more serotonin will act in the synapse. But people with this variant have
more antisocial behavior.
And if TH works better you should have more serotonin. But people with better TH tend to have more
impulsive violence.
So it's complicated, m'kay?
Where else do MAOb variants come in?
The New Zealand kids study.
The "good" version makes you less vulnerable to developing antisocial behavior.
The "bad" version (less effective at degrading serotonin, leaving more in the synapse) predicts more
antisocial behavior. With more aggressive childhoods, more antisocial behavior. Need childhood
abuse to make it happen. It's a vulnerability. Gene-environment interaction.
What effect does alcohol have on aggression?
Also see this play out with cultures newly introduced to alcohol. They adopt the drunken behavior of the drunken
role models of their colonial occupiers.
What are the two profiles of alcoholism?
Profile 1: Increases risk of antisocial behavior. Drinking socially. Men.
Reaching age 30 and you're cured.
Profile 2: no gender difference. Alcoholism most severe in late middle age. Barely functioning alcoholics
drinking alone.
Heritability separates out the two lines.
Acute environmental triggers of aggression: Releasing Stimuli

What are some primate releasing stimuli for aggression?

Stress, pain, and frustration.
Taking out aggression on those under you works out great for baboons' stress levels. Might explain something
about your future boss
Ex: rape seen in baboons in cases of displaced aggression after alpha male jerks are dumped off their thrones.
Does crowding cause aggression?
Hormones in adulthood influencing aggression

What does testosterone have to do with aggression?
SAME story as with T and sexual behavior
So elevated T within normal physiological ranges does not cause increased aggressive behavior.
Could you say T causes aggression?
No! It's about modulating aggression. Add T to the amygdala (and do nothing else) and it
doesn't fire more, but when it is stimulated from some other structure, far more likely to fire.
What is the challenge hypothesis for aggression?
T generates aggression when resources are being challenged.
But it also generates pro-social behavior if being pro-social is what it takes to defend resources.
More cooperation in the ultimatum game where you have to be prosocial to win money (a resource).
Who is our big exception to typical sex patterns in T and aggression? What are the patterns in this
exception?
Spotted hyenas.
Females have more androgens, have clitorises like penises, fat pads like scrotums.
Their social system has females on top. They also give birth to only 2 cubs. What do you predict for their feeding
order?
Now cubs go first, then females, then males.
Opposite of how it is in lions.
How do we explain PMS?
Some hypotheses about it being a myth, invented by the west, a "dependent" personality style, a conflict between
being productive and reproductive etc.
Bleh to all that. Baboons have the same profile of irritability/aggression so it's probably biological. AND males
have the same mood shifts along with female partners' periods so it can't just be the hormones.
So it's biology within a social context.
It might also be about depression. How could you explain that with hormones?
Drop in progesterone near the end of the cycle.
Progesterone potentiates GABA, as you should recall.
Opioid levels also drop around the period.

How does Lorenz' hydraulic model of aggression hold up to scrutiny?
It would say aggression is inevitable, and should be less likely after previous aggression.
But aggression is NOT inevitable. And aggression tends to beget more aggression.
How about the frustration-aggression Marxist hypothesis?
Holds up well. A lot like displacement theories.
Exception: aggression goes down during periods of famine, of scarcity. This would argue that
aggression is more behavioral fat.
How about behaviorist accounts of aggression?
This would predict it's all about reinforcers: rewards and punishments. That will determine
aggression.
Sort of true: premeditated crimes are influenced by penalties. But crimes of passion are not.
Human infants develop ego boundaries, theory of mind, self/other distinctions.
These as precursors for empathy and pro-social behavior.
Necessary but not sufficient, as seen with sociopaths who have great theory of mind
Does violent TV make kids more aggressive?
How do you respond to the claim that violence is biologically predetermined, since aggressive
violence peaks in adolescent males?
You'd bring up the data comparing murder rates in Chicago/Toronto/London.
They all follow the same rates of violence curves.
But the absolute amount of violence is hugely culturally determined.
Take-Home Point: your long-term environment teaches you the social contexts that are appropriate for violence.
Huge predictor of violence: living in a culture that rationalizes violence

How does the pattern of amygdala activation change in persons suffering from major depression? (2 pt)
________________________________________________________________________
a. According to what you learned in Bio150 about aggression, which of the following could be an explanation
for increased aggression (circle all that apply, 5 pts total, 0.5 pt for each):
a) Tumor in amygdala
b) Lesion in amygdala
c) Lesion in INAH3
d) Increased basal metabolic activity in frontal cortex
e) Lesion in septum
f) Enlarged anterior commissure
g) Stroke damage to frontal cortex
h) Increased dopamine release in nucleus accumbens
i) Decreased sensitivity of testosterone receptors in amygdala
j) Increased basal metabolic activity in anterior cingulate
b. You conduct the appropriate tests for the explanations given above, but fail to find anything wrong with the
brain structure, brain chemistry, or endocrine parameters in this patient. You decide that he could have a pre-
existing genetic tendency and that perhaps a modulatory environmental effect could have increased his
aggression.
Which of the following are environmental factors that could increase aggression by having a modulatory effect
on a pre-existing genetic tendency (circle all that apply, 0.5 pts each, 3 pts total):
a) Living in a rural area

b) Being an alpha male and having just lost a fight to the #2 male
c) Having a particular version of the MAO enzyme
d) Drinking large quantities of alcohol

e) Increased sensitivity of testosterone receptors in amygdala
f) Being subjected to child abuse
c. After more extensive physical and psychological tests and background checks, you conclude that this patient
is 100% fine. No pre-existing genetic tendencies towards aggression, no environmental factors, no biological
basis. Despite killing 34 people, no criminal charges are pressed against him. Given what you learned about
aggression in class, why might the man have killed 34 people? (1 pt)
Things to know for aggression

Some features of human aggression and affiliation that are unique to us, some that are less so than people used to
think.
What the amygdala and frontal cortex have to do with these behaviors (in a fair amount of detail).
The role of the anterior cingulate in pro-social behaviors.
Just a little bit about serotonin and aggression.
What alcohol does or doesnt have to do with aggression.
Some of the most common releasers of aggression.
Testosterone, estrogen, progesterone and aggression (in detail).
Some major theories about the broad nature of aggression.
Teaching of context, not how to be aggressive.
What Kohlbergs work is about and whether it actually predicts brave, moral behavior.
A bit about whether prenatal androgen exposure masculinizes aggression in human females.
Examples of gene/environment interactions regarding aggression.
Some ecological and anthropological predictors of levels of aggression in different cultures.
How do evolutionary principles regarding individual selection, kin selection and reciprocal altruism increase levels
of aggression?
How do the same factors decrease levels?
Pseudokinship, pseudospeciation, aggression and affiliation.
What circumstances in game theory play favor the emergence of cooperation
Aggression III
What are Kohlberg's three basic stages of moral development?
1. Preconventional: concerned with what punishments and rewards follow a behavior.
2. Conventional: concerned with the rules/laws/conventions to determine the morality of a behavior.
3. Post-conventional: concerned with some internal sense of right and wrong behavior independent of rules/laws
What are some issues with Kohlberg's stages?
Based on a non-representative upper class white male sample and there are gender differences.
Doesn't actually predict who does the right thing in real life. What does?
o Being raised with so much emphasis on doing the right thing that it's an internal,
implicit sort of behavior, NOT one that you have to think out logically.
So is moral behavior a matter of will or grace?
This has nothing to do with the TV show - do the readings! :P
It's about grace: doing the right thing (not lying) isn't a big effortful thing that you will to happen. It's about not
being tempted in the first place.
What does Judith Rich Harris teach us about the contexts in which we learn aggression?
It's all about the peer group and peer socialization. Less about parents (even absent fathers). Training in arbitrary
distinctions of us vs. them.
Ex: chimps vs. gorilla actors from Planet of the Apes formed dichotomous social groups.
What's a good predictor of having nicer social groups in primates?
Having older individuals in the group who are models for reconciliation behavior.
What about your early life environment biases an individual towards seeing us vs. them distinctions
easily?
Just pointing out the categories. Like "good morning boys and girls."
You can overcome this by growing up with lots of contact with diverse people: contact
theory.
But what are two examples that counter contact theory?
o Rwandan genocide with intermixed Tutsis and Hutus.
o Summer camps with Palestinian and Israeli kids: have the same prejudices but have
complex rationalizations on how the kids they know are different from the rest. So it
takes more contact than one summer.
What else about early life environment might bias an individual towards a life of crime/aggression?
Being born unwanted.
o Leavitt and Donohue found that 50% of the variance in the drop in crime in the 1990's could be attributable
to Roe v. Wade. Idea being that fewer "unwanted" children were born, and thus fewer crimes in adulthood.
Stress/poverty in childhood makes for a thinner frontal cortex with a lower resting metabolic rate leading to
worse performance on executive function tasks.
Witnessing violence in childhood
What important control-related brain region is developing during adolescence?
The frontal cortex is still myelinating up to age 25.
Supreme Court intelligently and stupidly made a cut-off that people under age 17 can't be executed for their
crimes, but the morning of your 18th birthday you suddenly can be. Breaking a continuum into buckets!
Also dopamine rewards fluctuate a lot more wildly in adolescence than in adulthood.
How does perinatal hormone exposure influence aggression?
What is fetal androgenization? How does/did it happen?
When female fetuses are exposed to high levels of androgens (like testosterone) during perinatal life.
Happens in cases of congenital adrenal hyperplasia (CAH) where adrenal glands pump out a lot of androgens, and
also in cases of exposure to diethylstilbesterol (DES).
What were the results in terms of aggression?
Overall, nothing very meaningful in the way it was initially interpreted. Originally interpreted as "more aggressive"
but that turned out to mean "interested in careers" and "less interested in dolls" than "normal" girls.
What were the results for other traits?
Higher IQ, though not when controlled with siblings.
Better spatial skills, higher rates of left-handedness, lower empathy and intimacy, potentially more aggressive
behavior. All of these are solid findings. But what's a big confound?
o Huge confound: born with ambiguous genitalia which takes a lot of reconstructive surgery and distress, and
also probably treated differently from non-androgenized girls.
What is the theory of autism as a hyper-male profile?
Autistic people have an exaggeration of traits that are male-typical patterns:
o Better spatial skills
o More systematic-based strategies for problem solving (as opposed to empathy-based approaches)
o Worse verbal skills
o Worse social cue reading
o Worse theory of mind
o Lower tendency to read facial expressions by looking in the eyes
o Thinner corpus callosum
All of these with slight differences in the average and large overlap!! So autism might have something to do with
prenatal androgenization.
How do genes influence aggression?
Genes have something to do with it: aggressive rat strains and breeds of dog are enough to show that much.
What are "the genes related to aggression" usually doing in a direct sense?
Modulating pain thresholds
Making a rat better able to detect the pheromone of a competitor
Or just genes for higher general levels of arousal (including affiliative behavior)
What are some candidate genes for aggression? What are the issues with the studies?
Review: MAO (monoamine oxidase) degrades serotonin in the synapse. Allelic variants of MAO are associated
with various profiles of aggressive behavior in humans.
o But remember, its a gene-environment interaction. The "bad" version only makes for more aggression if
it's coupled with childhood abuse.
Dopamine receptor genes come in allelic variants that have some association with aggression in adulthood.
o But these are actually more about impulsivity, sensation-seeking, and risk-taking.
How about XYY males?
o It was all a myth in the Richard Speck case. No evidence that sex chromosomal abnormalities predict
violence.
How does culture influence aggression?
Which traditional models of subsistence show the highest aggression?
Pastoralists most likely to have a warrior class than farmers or hunter-gatherers.
Pastoralists tended to colonize the American South. What violence patterns do you see in
the South?
o It's a culture of honor. And when honor is at stake, that's where violence comes out
(at much higher rates than in the North).
Low threshold for perceiving an insult
Culture of readily responding to insults with violence
Loss of status if insults aren't responded to
More guns
Little punishiment for violence in response to insults to honor.
Humans from which ecological systems are more violent? What other things are associated with
them?
Desert dwelers more violent than rainforest dwellers.
Desert dwellers also:
o Monotheism
o Top-down despotic leadership
o Leaders believed to be appointed by god
o More warrior classes
o More likely to aggrandize death in battle
How do we see different cultures play the ultimatum game?
University students across the globe all want to punish lousy, unfair offers.
But some did anti-social punishment where they punish those who make overly generous offers. Where did this
happen?
o Very low in Boston. More often in Greece, Muskat, S. Korea. Low social capital in these countries.
Interpretation: I don't want pressure from these angels to be a good person myself, so I'll punish their
generosity.
Aggression IV
Bedouin proverb: Its my brothers and my cousins against the world; its my brothers against my cousins.
How does evolution influence aggression?
What's the biggest sources of violence in animals (including humans)?
Competition over reproductive access including status/hierarchy position. Makes loads of sense from an
individual selection standpoint.
Interestingly and scarily, rape in humans seems to be more about power and control than reproduction.
But in orangutans, rape is an alternative strategy where subordinate males increase their reproductive success.
Competitive infanticide too
How does evolution help us explain chimp proto-warfare? What exception do we face?
Bands of brothers are exercising kin selection when they team up and annihilate
neighboring, unrelated male troupes.
o BUT bonobos are also patrilochal and they just have sex all the time instead of
genocide. Interpretation: who knows!?
What patterns of aggression exist in humans as a function of relatedness? How do we make sense
of them?
Child abuse more likely by fathers, paternal grandfathers than mothers or maternal grandfathers. Child abus eby
stepparents more than biological parents. Interpretation: less certainty about paternity makes for more violence,
almost like competitive infanticide.
But the data lends itself to economic interpretations as well, and hasn't been replicated well. So it's iffy on this
one.
What feature of human kin recognition predisposes us to pseudospeciation and pseudokinship?
The fact that we use cognitive strategies to recognize relatives means that they are susceptible to manipulation.
Examples of pseudokinship:
o Warriors among Masai cement pseudokinship by using kinship terms for each other and living together and
sharing food.
o Israeli military: groups of friends can join as a unit. They've been together since
kindergarten and feel like kin.
o WWII and Civil War both had cases where people were fighting against an enemy
that may very well have been more related to them than their allies in battle.
And how does this work in the realm of pseudospeciation?
o Making the enemy seem so foreign and evil that they hardly even count as human, hardly count as the same
species.
o Example: Gulf War as a result of the concocted Iraqi incubator story.
How does evolution influence non-aggression?
What's the alternative reproductive strategy for males besides being aggressive towards
competitors?
In pair bonding species we have lots of paternal parental investment
Females also choose nice males. So cooperating and being altruistic and generous can pay off in terms of
individual selection.
What examples do we have of pseudokinship making for affiliative behavior?
Rival Bedouin clans make peace and the "discover" a historical ancestor, providing plausible kinship ties with an
enemy.
Australian Aboriginal groups: when strangers encounter water in the desert, the concoct a relationship based on
family pedigrees so they can feel comfortable that the other won't try to kill them over the scarce resources.
Modern governmental propaganda: Nixon opens China in 1970's and so much emphasis came out on the
similarities between Chinese and Americans.
What activation patterns does the amygdala show for members of another race?
At first it looked like it just activated when viewing members of another race, but it turned out to be more
complex than that.
It DOESN'T activate in what three cases?
o The individual was raised in a diverse neighborhood (contact theory)
o The individual has close friends of that race
o You try to discern the person as an individual (does this person like Coke or Pepsi?)
instead of as a member of a group (is this person older or younger than 30)
What does game theory have to say about aggression and cooperation?
The Nash Equilibrium following a Tragedy of the Commons situation would predict that everybody defects all the
time for maximal gain.
But we do get cooperation, and it can pay off well (tit for tat, forgiving tit for tat, etc).
How does that cooperation get started?
Kin selection with the founder effect is the big theory here. Or just normal kin selection without isolation.
What eight other mechanisms foster cooperation?
o Repeated interactions
o An unknown number of rounds (not a finite set number)
o Reputation/open-book play
o Pairs playing multiple games at the same time (cooperation in one bleeds over to
cooperation in another)
o Altruistic punishment (policing - individuals can pay to punish cheaters)
o Altruistic rewarding (individuals can pay to reward altruists)
o Second-order punishment: punishing of non-punishers (like where you get punished
if you fail to report somebody else's honor code violation)
o Choice in who to play with
What's the take-home point on group selection?
It can exist in that groups of cooperators can outcompete groups of cheaters.
BUT that can have "good or bad" valence:
o Cooperating groups might communally raise children and that's lovely.
o Or cooperating groups might band together and exterminate neighboring groups (like with chimps). Not so
lovely.
And what are those two crazy situations where cooperation is the last thing you'd expect, but you
see it?
Christmas truce during WWI
Restraint from aggression with cooperation across trenches during fighting in WWI.
Depression
What behaviors/symptoms are associated with aggression?
Anhedonia
Grief and guilt
Psychomoter retardation (despite a hightened internal stress response)
Abnormal cognition and thought like memory issues, cognitive distortions (like seeing ambiguous faces as sadder,
or seeing an unrealistically pessimistic interpretation of the world).
Rumination where the frontal cortex is less active and people/animals perseverate in doing the same non-
functional behavior over and over
Suicide and self-injury. How does this play out in terms of gender and progression through depression?
o Higher "success" in men with suicide
o Higher rates of attempts in women
o Most dangerous time for this: when "coming out" of a super deep depression.
Interpretation: in the deepest of depressions there's no power to take an action or
control over the situation, but when the symptoms are improved just enough that
the individual can take action in the world but is still feeling terrible, that's when
suicide is most common.
Vegetative symptoms:
o Elevated GC load/stress level
o Elevated sympathetic tone
o Early morning wakening
o Disrupted sleep architecture
o Food intake disruption
Health consequences:
o Shortened life expectancy, even controlling for suicide.
o CV disease, diabetes, chronic inflamation. Why would we get these?
Could be due to different health behaviors like worse diet and poor exercise routines.
o Telomeres are shorter in those with chronic stress including depression
What are the different subtypes of depression?
Reactive depression: happens in response to some life event
Endogenous depression: happens because of some internal chemical malfunction
Unipolar depression: standard major depressive disorder
Bipolar depression: basic depression but also with cycles of mania (faster, more euphoric, sometimes bordering on
insane).
Where does the DSM play into this?
The Diagnostic and Statistical Manual is used in psychiatry to define what's normal and what counts as a disorder.
The line between what's a "normal" period of grief following a terrible event vs. abnormal shifts a lot.
Mostly in response to insurance and drug companies in what they'll pay for.
What are the demographics of depression?
15% lifetime incidence
2x rate in women vs. men for unipolar depression. No difference in bipolar.
In 25 years it will be the second leading cause of disability on earth.
High rates of drug-resistant depression
It's becoming more prevalent over the last 50 years, and it's NOT just a reporting confound
What is the neuroscience behind depression?
What are the three main NTs implicated in depression?
Norepinephrine, serotonin, and dopamine
What seems to be the case for each of them?
Norepi
o MAO also breaks down norepinephrine. MAO inhibitors treat depression.
o Reserpine degrades norepi vescicles and can trigger depression.
o Post-mortem examination of brains from depressed people show lower levels of norepi than normal.
o So it seems like it's a problem of too little norepinephrine. Tied to the psychomotor retardation symptom.
o BUT: MAO inhibitors work molecularly within hours but they don't improve depression for weeks. So it may
have to do with autoregulation and even opens up the possibility that it's too much norepi.
Serotonin
o Prozac and other selective serotonin reuptake inhibitors have the same issues with time-course as norepi
and MAO inhibitors.
o Tied to the rumination/perseveration symptoms.
Dopamine
o Central to pleasure, so maybe has to do with this anhedonia sympsoms.
But then what other neurochemicals are implicated in depression and in what way?
Substance p has to do with pain pathways, a possible link to psychic pain
Inflammation triggers sickness behavior which is really similar to psychomotor retardation and lowered mood.
CRH neurons project to midbrain structures and brainstem nuclei that activate the sympathetic NS. That's where
the stress part comes from.
BDNF is abnormal in depression too: important for neurogenesis and neural complexity.
[previous notes based on lecture notes. Subsequent material below based on notes from the Zebras chapter]
Neuroanatomy of depression
Cortex involved in depression because of abstract depressive rumination. Cut the connections between the FC
and the limbic system and you're good to go. This is the anterior cingulate cortex (ACC).
ACC responsible for recognizing negative emotional content in pictures
Resting levels of activation higher in depressives.
Amygdala overactive in depressives, especially toward sad faces.
Left PFC for happy. Right PFC for sad. More right PFC activation in depressives.
Genetics and Depression
Depression runs in families
50% concordance in twins.
We've found actual genes though
Immunology and depression
Being sick can be depressing
Chronic infections or autoimmune diseases are more likely to cause depression than other prolonged illnesses that
don't involve the immune system.
Cytokines released by the immune system interact with norepinephrine, dopamine, and serotonin systems.
Endocrinology and depression
Too little thyroid hormone is psychomotor retardation as well
Sex difference in women suffering unipolar depression more than men because they ruminate a lot more.
Depression's also about lack of power and control and women have less of that
Or estrogen and progesterone - more depression around menstruation, menopause, when taking the pill
How doe stress interact with the biology of depression?
Stress, GCs, and the Onset of Depression
o Stress and depression go together. Extreme stress often leads to depression.
o Having 3 or 4 episodes of depression makes you no more likely than anybody to have another, but at 5 or 6
you slip into a cycle that repeats.
o Depression AND GCs can raise the pleasure threshold. Prescribing GCs makes more depression.
o Having the bad gene only increases risk of depression with more highly stressful events during formative
years
GC profiles once a depression has been established

o Overactive stress response and stress hormones levels in depressives.
o Feedback resistance in HPA axis - more GCs secreted
What are the consequences of elevated GC levels before and during a depression?
o GCs affect serotonin, norepi, and dopamine. Abnormal GC levels can lead to abnormal NT levels - those
ones.
o GCs can damage hippocampus. Depressives have hippocampus problems.
Ant-GCs as antidepressants
o Going through depression is really stressful and stimulates GC secretion. So GC eleveation can be a cause or
a consequence of depression.
o Lower GC secretion and depression goes down. Block GC receptors in the brain and depression goes down.
Stress and the Psychodymanics of Major Depressions - Freud
Freud answering why some people fall into depression. Depression is an internal conflict generated by
ambivalence to what you lost.
Also about guilt for being happy about loss (of somebody's life or something).
Aggression turned inward
Stress, Learned Helplessness, and Depression - yay cognitive psychology
Loss of control and predictability, loss of outlets for frustration, loss of support, perception of life worsening. All
stressful. Give all these to animals and they get depressed.
Like the dogs or rats you completely stress out, they give up and don't avoid painful shocks anymore. They've
learned helplessness.
o Loose interest in sex and food and bathing. Psychomotor retardation, self-mutilation. Sleep loss.
o You can treat learned helplessness with ECT and antidepressants.
Humans can be provoked into learned helplessness with studies with inescapable loud noises.
The more internal psychological control, the less depression in humans.
If people learn that they cannot be loved or they cannot learn something or cannot do something, they develop
learned helplessness and are more vulnerable to depression. This could explain the early stressor=more
depression thing - you lose things you count on all the time like parents, then you're more helpless.
Attempting an Integration
Psychological approaches give insight.
o Loss of control
o No outlets for frustration
o Internalized battle of ambivalences.
o Aggression turned inward
Biological approaches
o Abormal NT levels
o Abnormal hormone ratios
o Genetic vulnerability
Stress brings them together.
o Psychological stress = learned helplessness
o GC levels up = depression up
o Anhedonia, psychomotor retardation, appetite, sleep patterns, feedback problems with GCs
But what about the 5-6 depressive episodes = a repetitive cycle unlinked to depression?
Why the individual differences even given really similar backgrounds and stuff?
o How dow e avoid getting depressed?
o We have recovery mechanisms built in. In most of us, the depletion of norepinephrine and serotonin is
transitory.
o Big synthesis:
Bad depression gene is in 5-HTT, a serotonin transporter.
Acted on by SSRIs.
GCs help regulate how much how much 5-HTT expressed.
o A big interaction of biology and experience.

Things to Know for Depression
The broad symptoms.
Know (in some detail) the evidence that depression is a biological disorder.
Which neurotransmitter systems are functioning abnormally in depression, what is the evidence for such
dysfunction, what are the functional consequences of those abnormalities.
The relationship between reproductive physiology and depression in women.
What does stress have to do with depression? Know this on multiple levels (epidemiological, endocrine,
psychological, genetic.).
What learned helplessness is about.
Schizophrenia
What do the behaviors of schizophrenia look like?
Is schizophrenia a disease with hidden blessings?
Not really, no. Comes with misery and suicide and social isolation
What are the positive symptoms?
The symptoms that most people don't have but schizophrenics have MORE of
Loose associations in thinking patterns
Extreme concreteness of thought
Delusions (especially paranoid ones)
Hallucinations (usually auditory)
Disordered sense of self and action (they can't tickle themselves)
What are the negative symptoms?
o Social isolation
o Emotionally flat
o Elderly have more negative symptoms than positive symptoms
Is disordered thought caused by the delusions/hallucinations first?
o Seems like they aren't causally connected because drugs can take care of the delusions/hallucinations but the
disordered thought symptoms are still present. So they're independent symptoms.
What's the demography of schizophrenia?
o 1-2% worldwide. No culture bias. No gender bias.
o Onset is usually in late adolescence
o No SES bias in incidence, but once you get schizophrenia, a SES downward spiral often follows
What is the neurochemistry and brain metabolism of schizophrenia?
What are the three NTs implicated?
o Dopamine, serotonin, glutamate
What's the evidence that schizophrenia is a disease of too much dopamine signaling?
o First, this could mean that there's too much dopamine NT floating around OR that the post-synaptic neuron is
more sensitive to dopamine
1. Antipsychotic drugs like thorazine and haldol decrease schizophrenic symptoms and their mechanism is too block
dopamine receptors
2. We see a lot of dopamine breakdown products in CSF, blood, urine
3. We see more dopamine receptors in some post-mortem studies of schizophrenic brains
4. Some studies show that schizophrenics are more responsive to drugs that have dopamine-like actions
5. If you treat Parkinson's disease (disease of TOO LITTLE dopamine) with drugs that raise dopamine levels, you get
schizophrenia-like side effects. And vice versa (inhibit dopamine signaling to treat schizophrenia and you can get
Parkinson's-like symptoms).
What's the evidence that schizophrenia is a disease of too little dopamine breakdown?
Idea being that dopamine levels are fine, but when they come off the receptor, the COMT enzyme is not working
properly, and dopamine is not degraded. Too much is left in the synapse.
Complicating our measure of dopamine breakdown product in the urine, how can it be that
enhanced dopamine signaling could produce abnormally high, normal, or abnormally low dopamine
breakdown product levels in the urine?
Too much dopamine signaling in the synapse leads to:
o
Clinical finding Cause of enhanced dopamine signaling
Low breakdown product COMT enzyme is broken

Normal breakdown product Just too many or too sensitive of receptors for dopamine
High breakdown product Too much dopamine released
What's the neurological logic connecting dopamine to schizophrenia symptoms?
Unclear, but probably not about pleasure/anticipation.
Probably something with mesolimbic dopamine projections into the frontal cortex, somehow disrupting executive
function and logical, sequentially ordered thought
What's the evidence implicating serotonin in schizophrenia?
Hallucinogenic drugs (LSD/acid, mescaline, and psilocybin/magic mushrooms) are
basically exogenous serotonin and they cause hallucinations just like in schizophrenia.
Blocking a serotonin receptor relieves some of the negative symptoms of schizophrenia
And the evidence implicating glutamate? (Not a whole lot)
Drug called phencyclidine (PCP/angel dust) can produce a psychotic state similar to schizophrenia and it works on
glutamate pathways.
Preadolescent children (who can't get schizophrenia) also can't be made psychotic by PCP. I'd like to see the
informed consent for that experiment...
What are the structural and cellular differences in the brain in schizophrenia?
Why is it hard to even get answers to these questions?
You often need VERY recently alive brains to cut up, stain, etc. to measure brain and cellular structures. Hard to
get. When you take brains out you squish them too.
Other problem: schizophrenics often have poor nutrition, vitamin deficiencies, and also take tons of drugs to treat
their condition. So you don't know if your findings are due to the actual brain abnormalities that caused
schizophrenia or those other confounds
How can you get around those issues?
Use brain imaging instead
Study unmedicated schizophrenics (esp. early on in the disease)
Study close relatives of schizophrenics who might have the same changes but to a lesser
extent.
Also clues you in to the genetics.
But regardless, what are the big findings in terms of the differences?
Larger ventricles (atrophied brain tissue)
Small loss of neurons in the hippocampus
Hippocampal neurons are oriented in the wrong direction

Frontal cortex has neuronal loss and structural atrophy
o Loss of GABA neurons (perhaps explains enhanced dopamine signaling)
o Remember that frontal cortex is still maturing ages 18-25 and that's also where you get schizophrenia
Glia distribution abnormalities
Reelin protein has abnormal levels: it helps neurons migrate appropriately
Some evidence for thalamus atrophy
What are the genetics of schizophrenia?
What do classical behavioral genetics approaches tell us?
Gotta remember Kety's study of schizophrenia in Denmark. Biological/adoptive parent associations and the
synergistic event of schizophrenogenic environment and genes.
Standard approaches (with standard caveats) show schizophrenia has genetic links: more concordance with closer
relatives.
Standard approaches also show schizophrenia has environmental components: DZ twins have higher concordance
for the disease than non-twin full siblings.
What have we learned from molecular genetics about schizophrenia?
Inconsistent genetic markers, probably because it's a heterogeneous disease.
COMT variant is associated with schizophrenia with a tiny effect.
o Interestingly, the version that broke down dopamine MORE efficiently was associated with HIGHER levels of
schizophrenia, complicating our earlier take on COMT and dopamine.
DISC-1 (disrupted in schizophrenia 1) is a gene that is, unsurprisingly, associated with schizophrenia. But also tied
to depression and bipolar disease too.
MHC genes seem to be disrupted in schizophrenia. (see below with viral infection connection)
Various genes show abnormal copy number variants in schizophrenia.
What role does early life experience play in schizophrenia?
There's only 50% concordance in MZ twins, so you know at least 50% of the variation is due to environmental
factors! Genes, again, are far from deterministic in this disease.
How do we know stress plays a role in developing schizophrenia?
Dutch Hunger Winter fetuses have 2-3x the schizophrenia incidence. Same with the
Chinese Famine of 1960.
Mothers with major complications during labor have children with higher incidence of
schizophrenia.
Stressing rats prenatally causes more dopamine releasing terminal density in the frontal
cortex
Does being schizophrenic make you more at risk for viral infections?
No, seems to be the opposite: viral exposure often precedes the onset of symptoms
Perhaps immune defenses against pathogens work differently in schizophrenia (see above for MHC link)
Which parasite is specifically implicated?
Toxoplasma gondii: exposure precedes onset of symptoms.
Can parenting style be schizophrenogenic?
No evidence! Despite a long history in psychiatry of telling mothers they caused it with their "conflicting emotional
demands along with a cold, aloof style."
But what link do families where some members have schizophrenia share?
This subtle communicative style: telegraphic/vague communicative patterns that everybody understands perfectly
in the family.
Descriptions of inkblots are readily understood between family members where schizophrenia has some influence.
Caveat with all this: "There is no particularly satisfying model at this point that integrates the genetics, neurobiology,
developmental features and symptoms of schizophrenia." -extended notes
How do we understand the evolution of schizophrenia?

Is schizophrenia adaptive?
Absolutely not. Fewer offspring, shortened life expectancy.
What might be adaptive about it?
Minor point that there might be less cancer in schizophrenics.
Major point (see religion lecture) that schizotypal personality (having a partial version of
schizophrenia) can be quite adaptive.
The Biology of Religion

What tend to be the basic behaviors/experiences of religion? (some are shared, but lots of
variability too)
Paranormal/meta-magical belief: faith in things that cannot be verified or seen or are outside material human
existence
Ritualism
Finding of patterns, searching for agency and causality in the patterns of the natural universe
Emphasis on religious philosophy
Emphasis on faith
The point being that many aspects of religion and religious belief have biological explanations just as much as any
other human behavior (including non-belief! It's just not studied as much so is less included here).
Schizophrenia and meta-magical belief
Back to schizophrenia. How do we explain schizophrenia's evolutionary fitness?
NOT that schizophrenia is an adaptation.
But schizotypalism (an intermediate/partial form of schizophrenia often seen in relatives of schizophrenics) can
actually be adaptive. How so?
o Throughout human history, these tend to be the medicine men/women, the
shamans wrapped up in meta-magical thought. They hear voices at the right time.
o In small numbers, they're helpful to society.
o They tend to leave more offspring
And behaviors/features typify schizotypalism?
o Meta-magical thought (converse with the dead)
o Concreteness (he literally did walk on water)
o High degree of religious belief
o Social withdrawal (not so far as isolation as with schizophrenia)
o Do the trances, conduct the ceremonies, fast for 40 days in the desert, etc.
o Perhaps invented some of the more fantastic stories passed down in religious cannon
Our Western, US culture is totally rational and beyond all manner of magical thinking, right?
Hellz no!
25% believe in ghosts. 37% in telepathy. 47% in UFOs that have interacted with humans. >50% believe in Satan
who plays a role in people's lives.
Big theme: get your religious/magical thinking at just the right level, and it can take hold in society and even have
fitness advantages. Take it too far and it's a cult or schizophrenia. But just right and it's schizotypalism and
religion.
OCD and ritualistic practices
First, what is OCD? What are the behaviors, the thoughts, the condition?
A very intense, pathological disease in its full form. Not the minor obsessions/compulsions that affect most
individuals.
Spend many hours a day doing compulsions: behaviors that the individual has almost no control over. Like
washing, door lock-checking, etc. to a pathological degree.
These compulsions in some sense assuage a deep anxiety and dread about the world (germs, theft, etc.)
A mental component: obsessions. Thought patterns that you can't escape, obsessions with counting things, with
certain numbers or arrangements of things.
Obsessions and compulsions usually focus on these four things:
o Hygiene
o Food preparation
o Entering/leaving a building/space
o Numerology/symmetry
In what way does religion also show some of these characteristics? What are some examples?
Hindu Brahmans do hours of washing and prayers every day. Society supports them in this endeavor.
There are certain magic numbers in many religions, particularly Orthodox Judaism: 613 rules. And the numerology
itself is the point, less about what the rules are. Same with Islam and Christianity.
Many religions have doctrine around hygiene, food preparation, entering/leaving, and symmetry.
Martin Luther's writings clearly suggest OCD, and he was clearly tremendously influential in shaping religious
history.
Interpretation: many religious rituals may have resulted from the influence of OCD in the past.
Interpretation: religion is a sanctuary that supports these behaviors, gives them a context in which they are
adaptive. In other contexts they'd be considered straight up psychiatric disorders.
o Ex: you can be a kosher certifier and make a living just making sure that food is prepared in the right way.
o Ex: anorexia nervosa is clearly a disease in one context. But Catherine of Sienna was comforted and
supported in anorexic behavior as saint-like and divinely inspired.
Religious Faith and Explanations of Causality and Agency
Humans tend to infer agency and causality even in inanimate objects moving around on a screen. We also look for
agency and causality in the universe and in the realms of life that are most mysterious/unknown (time, eternity,
death, consciousness).
And if there's no proof, that's okay. Many religious emphasize the importance of faith itself: believing things
because of the belief, not because of the evidence for the belief. Opposite in science.
What kinds of gods to humans tend to have?
Familiar, recognizable gods in the image of humans.
Gods that have faults and affairs and trickery (just think of Greek mythology).
And then we get Judaism and a monotheistic god that is unknowable, hidden, omnipotent, and with desires that
humans can't even fathom.
What experiments led credence to the idea that humans tend to see patterns when there are none?
Superstitious behavior can be triggered even in pigeons. Reward them randomly, and
whatever behavior preceded that reward, they will perseverate in doing even though it
has no causal connection to the reward.
Humans tend to see patterns in random data that don't actually exist, and it's MORE
LIKELY when they've just been doing a task in which they have little control over a reward
outcome.
What personality type is more likely to lean towards religiosity?
Intuitive personality.
And when you prime people to think more analytically, they tend to express less religiosity and more disbelief. 3
experimental examples?
o Like making them look at The Thinker statue instead of a discus thrower.
o Like priming with random lists of words. One set has words like "think, rational,
ponder" thrown in there.
o Like reading a paragraph in a font that's very hard to read: you have to analyze the
letters to read it.
Philosophical religiosity
Epilepsy in the temporal lobe (activation) leads to what outcomes?
Hyper-seriousness
Perseveration: sticking with ideas/patterns
Dislike of new things
Hypergraphia: obsessive writing
Concern with the philosophical features of religion (not necessarily religious belief itself)
Genetics and Evolution

What are the demographics of religious belief?
Less than 2% identify as atheists. A few more identify as agnostic.
So religious belief is almost universal.
EXCEPT in Scandinavian countries where >50% are now atheistic.
Also recall the ecological correlates of religion: deserts with monotheism, rainforests with polytheism.
How does religiosity correlate with size of group?
The larger the group, the more the chief religious entity is emphasized to be monitoring behavior. Kind of serves
as a policing force of sorts.
How does it correlate with SES distribution?
The more income inequality, the more religiosity. Esp. ritualistic versions.
Interpretation: lack of control and inequality in a given context leads to satisfying rituals and the promise that the
meek shall inherit the earth.
And my (Steven's) apologies to my diligent section-handout-readers, but I had to peace out 10 mins before the end of
this lecture so you should be sure to review the final points from your own notes.
Final Lecture
This one is all about where we draw the line between "normal" and "abnormal" behavior; it's about where fault should
lie for behavior; it's about wrapping up the myriad influences on human behavior.
In what way do we know think of epilepsy in terms of volitional control?
There's clearly a disease and there's clearly the person. And those are two different entities even though they
both influence behavior.
We're pretty good about understanding this line with epilepsy and generally with schizophrenia. Less so with
dyslexia, depression, or frontal cortex damage.
Two examples of impulsivity/inhibition and the frontal lobe:
1. D2 receptor variants make for differences in risk taking/impulsivity/sensation seeking. But the context in which
this plays out is widely variable (base jumping vs. chess playing).
2. Before the motor symptoms of Huntington's disease comes disinhibition of the frontal lobe. This actually leads to
people with Huntington's to outreproduce their siblings during this period, providing an individual selection
mechanism that explains the persistence of this disease.
What are the symptoms of Tourette's syndrome?
Twitches, ticks, body jerks, sounds, barking sounds, rhythmic coughing, grabbing at body parts.
How have we as society changed in how we view the disease?
Used to be burned at the stake or exorcised for doing those things. Now we know it's a disease and try to
accommodate it. We've drawn a line between the person and the disease.
What evidence do we have that Tourette's might be related to autoimmunity? PANDAS disease.
Kid gets strep infection, along come ticks and other Tourette's symptoms
Immunosuppressants take the symptoms away.
When you get sick again, the symptoms return along with high fevers
Interpretation: maybe the high fever opens up the blood-brain barrier and the immune system attacks the brain.
And what brain region is implicated?
The caudate: seems to be abnormally small in Tourette's
And then there's the endless variety of bizarre and surprising disorders resulting from our biology. I would just be
repeating what Dr. Sapolsky said word-for-word, so I'll skip those and leave them up to you to review.
Will advancement of science rob the universe of all mystery, wonder, and meaning?
Yes. Jk. No.
Take-home points:
Life is complicated and bizarre and more mysteries open up with every discovery.
We as a society suck at understanding human behavior and its biological underpinnings.
Biology can be woefully mis-applied when done incorrectly (Lorenz, etc.)
Just because it's complicated, that's no excuse to do nothing.
You don't have to choose between science and compassion. You can do both.

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Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012.

Background from section

Introduction and Evolution/Sociobiology

Pros and cons of categorical thinking

Five pieces of evidence for evolution?

How do you calculate degrees of relatedness?

What typically characterizes species that demonstrate reciprocal altruism?

Pair Bonding and Tournament Species

What are some further behavioral examples explained well by sociobiology?

or 4th cousin matings produce the most fertile offspring.

Group selection. Is it valid? What version is invalid?

What are four criticisms of sociobiology?

Example Exam Questions

- How would a sociobiologist justify the existence of parent-offspring conflict over

For our purposes, what is the central dogma of life?

What are the three types of mutations in classical genetics?

*What do we mean by microevolutionary vs. macroevolutionary change?

Four examples of a microevolutionary change having a big impact on behavior?

What is the 95% of DNA that doesn't code for proteins?

How do you know when to express certain genes?

Overall, this is the concept of if-then clauses.

What's 1 molecular mechanism and 1 example of epigenetic regulation?

What do transposons do and where do we see them play out in nature?

What's the molecular mechanism of PE changes?

What about the mechanisms for the stasis part in PE?

How can you get multiple proteins from one gene?

How did the prairie vole example show these principles?

Who wins in the end? The gradualist creeps or the PE jerks?

Example exam questions

What 3 important things happen in the pre-natal environment?

How do behavioral geneticists hone in on actual genes?

What does heritability tell us?

How do we know if something is highly heritable?

Which of the following show high heritability?

Example exam questions

Percentages in the table above represent the

a) Give three examples of this principle from class. (6 pt)

What's the difference between statistical significance and functional significance/importance?

In what ways do species recognize relatives?

Positive punishment Decrease likelihood of repeating a

Ethology is then about a few basic questions

What in the external world caused the behavior?

The sauce barnaise syndrome and one-trial learning

Hyp Hypothalamus (brain structure)

Pit Pituitary (brain structure)

CRH Cortocotropic Releasing Hormone (from hyp to pit)

ACTH Adrenocorticotropic Releasing Hormone (from pit to adrenals)

GCs Glucocorticoids (stress hormones from adrenals to body)

VP Vasopressin (hormone from pit to body and from hyp to pit)

OT Oxytocin (hormone from pit to body)

What complexities do we have at the level of NTs?

o Different speeds of action: fast excitation followed by slow inhibition

Autoreceptors doing bookkeeping

What complexities do we have in how peptide

How do the hippocampus and amygdala mediate fear memories?

Example Exam Questions

Why is that? (2pts)

Reductionism and Chaos

i. Illustrated with cellular automata and their interactive reproduction rules.

2. Like Sapolsky's testosterone meta-analysis

Emergence and Complexity

What are the components of true emergence? Very important.

How does emergence apply to humans?