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BIOL 273

Lecture 1
Course Outline

Lecture 2
Multiple Choice Review Question
1. Which of the following allow the movement of gases (O2 and CO2) across the
epithelium?
a. Transport b. Exchange c. Ciliated d. Protective e. Secretory

Lecture 3
2. Receptor molecules for chemical signalling can be located
a. in the membrane b. in the cytosol c. in the nucleus d. b and c e. all of the above

If the receptor molecules are nuclear than they are inside, but for cytosolic and membrane they
might either be in the cytosol or on the membrane for it bringing it in, so its dependant on the
signalling molecule and its function

Nervous System Function


- Key control structure (along with endocrine)
- Receives information using sensory neurons (receptors) to receive from external
environment
o we have mechanisms inside our body such as specialized cells, like joints that
sense how we are moving
o there is a sensory pathway regardless of whether the information is being obtained
externally or internally
o a receptor is a cell that is capable of receiving information (used to describe an
actual cell rather than a protein inside a cell)
- Integrates information (organizes info. and brings together with already previously stored
information)
- Transduces information (sends appropriate signals to muscles or glands)

Two components of the nervous system: central (CNS) and peripheral (PNS)
- CNS: brain and spinal cord
- PNS: sensory neurons/receptors, efferent neurons

CNS Brain and spinal cord


- Clusters of cell bodies -> nuclei
- Bundles of axons forming a pathway -> tracts
(Always associate the terms nuclei and tracts as related to the CNS)

PNS Everything else


- Consists of nerves -> bundles of axons of sensory or motor neurons existing outside of
the CNS
- Receptors - Peripheral nerves - Clusters of cell bodies -> ganglia
Stimulus -> sensor/receptor -> afferent pathway -> integrating center -> efferent pathway ->
target or effector -> response
- Stimulus attacks the sensor/receptor which then carry on in a sensor/afferent path and
arrive at the CNS which receives this information and becomes the integrating center and
processes the information to a motor/efferent path which attacks a target/effector and
9yhy6creates a response to the original stimulus

Components of the nervous system


1. Receptors: are specialized cells that convert stimuli (eg. touch) into electrical signals and
transmit information to sensory/afferent neurons
(Eg. when you hear sounds, the hair cell in your middle ear are rapidly moving when
processing this sound deeper into your ear so it is this movement of the hair that creates a
signal: i.e. the stimuli is changed into a signal)

2. Afferent (sensory) neurons: transmit sensory information TO the CNS because these are
cell bodies that are located outside the CNS, and then long cytoplasmic extensions
transmit info. to cells (interneurons) within the CNS

3. MISSED THIS BC ON PHONE (URGH)

4. Efferent (motor) neurons: receive info. from interneurons, there are cell bodies located
within CNS and the cytoplasmic extensions transmit info. to effectors muscles and
glands (so its pretty much that you receive a signal that signal is interpreted within the
CNS and then sent out to a different area)

Concept Maps (very helpful in this course)


Nervous System
CNS PNS
Brain and spinal cord Sensory and motor
Somatic and autonomic
Sympathetic
and parasympathetic
The only target cell is a skeletal muscle when we are talking about the somatic motor neuron
For autonomic, the control is over smooth muscle and influences cardiac muscles, endo/exocrine
glands

Cells of the nervous system


a. Neurons b. Glial cells (neuroglia)

Typical neuron (nerve cell)


- Main role: transmit signals over long distances (this distance varies)
- 4 main parts:
i. soma (cell body): center of chemical processes (keeps cell functioning and alive)
Soma does mean body so you can interchangeably use the words cell soma and cell body
ii. dendrites (dendron: tree): transmit electrical signals TOWARDS soma
iii. axon: transmit electrical signals AWAY FROM the soma (when the cell becomes very
iv. axon terminals: participate as part of the synaptic (presynaptic) (NOTE INCOMPLETE)

Diverse neuron forms and functions


Pseudounipolar (pseudo uni polar : false one pole)
o somatic sensory neuron
o axon & dendrites fuse during development (one long process)
bipolar (bi polar : two poles)
o smell/vision sensory neurons
o single axon and dendrites (?) DIDNT FINISIH NOTE
anaxonic (dont worry about this too much the function is not very well understood)
o interneuron
o no apparent axon
multipolar CNS (multi polar : many poles)
o highly branched
o no long extensions for the axon
multipolar efferent (multi polar : many poles)
5 7 dendrites
single long axon

Glial cells
- Outnumber neurons by 50:1 -> they are associated with neurons (there are a lot more
glial cells that will help the neurons carry out the job of carrying electrical signals over
long distances)
- Dont carry electrical signals over long distances (communicate with each other and with
nearby neurons using electrical/chemical signals)
(NOTE UNFINISHED)

Two types: Schwann cells and satellite cells


1. Schwann cells -> wrap around axon
o forms myelin (myelin is just multiple layers of membrane wrapped around itself)
o gap junctions found between layers
o electrical insulator

2. Satellite cells
o non-myelinating Schwann cell
o support nerve cell bodies (soma)

Glial cells of CNS


- Oligodendria (oligodendrocytes)
o CNS version of Schwann ecell
o wraps around axons -> forms myelin to insulate axons
- astroglia (astocytes) -> small star-shaped cells (astron: star) (DIDNT FINISH THIS)
- microglia
o very small
o specialized immune cell (macrophage-like)
o function is to remove damaged cells & foreign invaders
- ependymal cells
o epithelial cells that produce cerebral spinal fluid (CSF)
o create selectively permeable barrier between compartments of the brain)

Lecture 4
3. Which of the following is/are sensory neurons?
a. anaxonic b. pseudounipolar c. bipolar d. b and c e. all of the above

How do neurons transmit electrical impulses?


- via energy stored as an electro-chemical gradient (utilizing this energy is very important)
- Need to understand the physics of electrical and osmosis as they apply to cells

Cell membranes are really good insulators that ultimately separate the ICF and ECF (intra and
extra cellular fluid)
- When the cell membrane separates those charges it creates an electrical gradient because
of the difference in charges that outside vs inside
- Coulombs law: you see a change in the strength as it decreases as it is further away from
the charges (the closer it is, the stronger it is)
- there are net negative charges on the inside and net positive on the outside (this is the
difference that creates a gradient, when the gradient involves these electro-chemical
charges it is an electrical gradient)
- the insulator (membrane prevents the charges from freely moving across the cell
membrane)
- you must create an ion channel to process movement of these charges because the cell
membrane is such a good insulator

Osmotic principles deal with a chemical gradient


- occurs when you have a difference in concentration across the membrane
- a concentration gradient is important because molecules move down the concentration
gradient which means they move from an area of high concentration to an area of low
concentration (this is important because this naturally occuring behavior of molecules
creates a free movement across the membrane as long as the cell membrane is premeable)
but from what we know, the cell membrane is semi-premeable

The semi-premiability means that some molecules are too big or too repulsive to pass through
the cell membrane so even though there is a concentration gradient set across the membrane,
which is pushing the molecules from a high conc. area to a low conc. area, these molecules must
be processed through protein channels (which are big openings in the membrane due to protein
interference which allows the specific molecules to pass across the membrane using that protein
channel)

influx and eflux (eflux is when you move outside, influx is when a molecule moves into the cell)
- for most molecules the cell membrane is impremeable too, so it is only through the ion
channels that it is able to move across that cell membrane
- no net movement means that there is no net influx or no net efflux of that ion across the
membrane (it doesnt mean that there is no movement at all)

For any given ion you can easily calculate the electrical potential of the cell needed to generate
an equilibrium state, if you know the concentration gradient

What does the nernst equation do? predict the equilibrium potential for an ion

(understand what the equation is used for, and be able to recognize the equation)
Equilibrium potential allows you to determine what the electrical potential will be when there is
no net movement across the membrane
z = electrical charge of the ion (eg. sodium ion has a +1 charge)

If you compare the actual membrane potential of the cell to the equilibrium potential for that ion,
you can predict whether an ion is going to move into or out of the cell

Membrane potential: at rest there is always a difference


ALL CELLS HAVE MEMBRANE POTENTIAL AND ALL CELLS ARE NET ELECTRO
NEGATIVE INSIDE THE CELL (but only the cells that are known as excitable tissues that will
utilize that membrane potential, which is what the major difference between signalling for the
nervous system cells and regular cells are)

The membrane potential results from the different concentrations of ions inside the cell
vs outside the cell

The excitable cells, when they are not at rest they are excited, we call this membrane potential
because having that electro-chemical gradient is a source of energy (a dam is no different than a
cell membrane, it is a great insulator which doesnt allow molecules to freely pass, when there is
a concentration gradient there is potential energy)
Think of a water behind the dam, there is water just waiting to flow out and burst so that
dam is the membrane and that water is at rest which has potential ENERGY

At rest a neuronal cell at sit at a -70 (which comes from the concentration gradient of different
ions across the membrane and their membrane premeability)

On the graph, for hyperpolarization, your starting point always has to be at rest (so the resting
potential), even when you are at a hyperpolarized state (what is it called when you return to rest?
repolarization)

Repolarization is from any starting point when you are returning to the original rest position

The light green is what represents the opening of the channel where as the dark green represents
the two poles that keep the membrane separated

CONCEPT CHECK:
Match each ions movement with the associated change in membrane potential
1. Na+ entry (D)
2. Cl- entry (H) Depolarizing
3. K+ exit (H) Hyperpolarizing
4. Ca2+ entry (D)

Depolarizing is you going towards move positive, hyper is you going more negative
So when you gain sodium, you go more positive which is depolarizing, when you lose potassium
or gain chloride (you are hyperpolarizing your cell)

Would a cell with a resting membrane potential of -70 mV depolarize or hyperpolarize in the
following cases:
1) Cell becomes more permeable to Ca2+ (Eion = +122 mV) -> depolarize
2) Cell becomes less permeable to K+ (Eion = -90 mV) -> depolarizes (the positive charge
of the K+ stays within the cell, so it makes the overall charge less negative)

Lecture 5

4. Q: T/F: Na, K, Ca ion concentrations are higher outside the neuron


False: K is greater inside

Role of sodium ions:


Na+ contribute minimally to resting membrane potential -> due to low permeability
- but very important in generating changes in membrane potential that causes electrical
signals

Graded potential

Depolarization (moving towards positive), hyperpolarizing (more negative; could be getting


more negative towards the resting membrane potential)
- occur in dendrites/cell body, open/close channels

It can be either strong depolarizing or strong hyperpolarizing, one or the other (not both)
- always strongest where it initiates but always loses strength
Membrane incomplete impermeable to the movement of ions (leaky channels: graded
potentials lose strength)

What causes a graded potential to start? neurotransmitter (signalling molecule that binds to a
receptor and opening ion channels)
- the ion channels are triggered by neurotransmitters (the binding to the receptor causes the
ion channel to open)
- strength of the graded potential ~ strength of the original stimulus and how many
K/Na/ions have moved through the channel causing a hyperpolarized graded potential or
depolarized graded potential
two neurons communicating with each other (synapse) and send chemical signal which causes a
Na ion channel to open (depolarizing effect because the Na(+) enters the cell, so where would
the graded potential be the strongest? CLOSEST TO THE ORIGIN OF THE STIMULUS

...if graded potentials travel only short distances how can a neuron that reaches the full length of
the body travel?
- essentially impossible for a graded potential to travel that distances in a resonable amount
of time without degrading (regardless of how strong the original signal, theres too much
leakage/resistance for the graded potential to travel the full length of the body)
- a different kind of signal is used: action potential (rapid long distance electrical
signal/impulse that travels down the length of the body)

Action vs graded:
two differentiations:
1. action potentials identical to each other: no volume control : they are on/off
- no slightly different graded strength (it is either happening completely or not at all)
2. action potentials dont diminish in strength as they travel long distances through neuron
(signal is strong all the way)

what triggers action potential? membrane potential (when resting membrane potential deviates
around -55mV, it is known as the threshold potential for the action potential to become triggered)
- the right spot to look whether the threshold potential has been reached is at the trigger
zone (if the graded potential has a depolarizing effect, at -55 does it initiate an action
potential? only if the -55 is at the trigger zone (because thats where it starts)
- even if it is strong enough to go past/reach the threshold, if it has decreases in strength by
the time it reaches the trigger zone then no action potential is fired

Graded potentials can initiate action potentials:


multiple axon terminals all possibly sending signals (could be either
depolarizations/hyperpolarizations) but it can happen all the way around the cell, so different
areas where the signals come from but they all come together and summate at the trigger zone
(and if they collectively have a potential minimum -55mV, then action potential is triggered)

Graded potentials can sum over: space (spatial summation)


(Regardless of how they summate the main question is whether the threshold potential is met for
the action potential to be intiated? is the stimulus strong enough to reach threshold at a distance
where the trigger zone lies?)
spatial summation: multiple synpases causing graded potential inside the cell and as those graded
potentials come together summate at the trigger zone
(minimum -55: three depolarizing graded potentials will reach threshold (or go above)

over time (temporal summation: where graded potentials occur in one single location, and follow
that signal location as time goes on, we can see multiple graded potentials and bring those graded
potentials together at the trigger zone to reach the threshold)
two graded potenaisl will not cause an action potential if they are far apart in time
- if two subthreshold potentials arrive at the trigger zone within a short period of time (they
may sum and create an action potential)

spatial/temporal summations can happen at the same time (temporal is a very strong amount of
time)

EPSP (exicatory post synaptic potential: signal that happens in the neuron (if depolarizing: it
excites the cell: it might not make it there but they increase the chance of exciting the axon to
fire an action potential (they might not meet threshold but it helps to atleast try to get close)

IPSP (inhibitory post synaptic potentials: overall membrane potential is decreasing so its getting
further and further away from the -55 threshold which causes the action potential to be inhibed)

depolarization triggers Na+ (activation gate closed) rapidly opens (activation gate open) and the
positive feedback loop continues
until something outside isnt happening (then inactivation gate gets corked in to stop)

how does the membrane potential return to resting level? K+ ions leave the cell
(falling/repolarizing phase of AP)

returning resting membrane potential: K channels are slower to open than Na+ channel ->
depolarization to threshold triggers opening k channel
(gating potential: i.e. full opening is around +30, compared to full opening at -55 for Na channel)
open: the activation gate is open, allowing passage
closed: activation gate blocks movement
the trigger for both the channels is -55 but the k channels just open so slowly that it is
around +30 mark that the K channel is fully open which is when we see the movement of
potassium inside/outside the cell

NOTE*** very few ions move across the membrane during a single action potential: the
concentration gradient DOES not change much after one action potential
(misconception: doesnt take very many to go across the membrane to change the membrane
potential)

Lecture 6
Q. The trigger zone in a neuron:
a. is at the axon terminal of efferent neurons
b. is a region of the axon called the final segment in efferent neurons
c. is the integrating centre of the neuron
d. a and b
e. a, b, c

Why cant AP (action potential) be generated during the absolute refractory period?
Na channel is in the inactive phase (you can generate one when it is in the closed conformation)
and that closed conformation only happens in the relative refractory period
-70 to -55 is the threshold stimulus, but during the relative refractory period the resting potential
might be sitting at -73, -74, so it is hyperpolarized, so to go from -74 to -55 takes more stimulus
(so this is called the suprathreshold zone)

The Domino effect:


electrodes have been placed along the axon
(once the dominoes have fallen over that is the absolute refractory period, because you cant
have another domino fall until you reset it:

memberance potentials are recorded simultaneously

If you cant propagate the action potential with a decent amount of speed, then it wouldnt be fast
enough which is a problem

Membrane resistance:
determined by diameter and leakiness of neuron:
there altering the diameter of the leakiness changes the resistance

Some invertebrates (squid and earthworm) have fairly simple nervous system but they are able to
control the resistance of the membrane
- they have GIANT AXONS
- which means that there is a great diameter (the greater the diameter, the greater the
reduction in the resistance)
When you reduce axon diameter, you increase the resistance

Vertebrates (because we dont have giant axons that can combat membrane resistance) we have
another way which is insulated nerve (remember nerve is just a bundle of axons)
insulated nerves:
- reduces resistance or degree of leakiness
- insulated axons speeds conduction

Mammalian neurons are surrounded by a myelin sheath:


- myelin sheath acts as an insulator
- it is made up of many layers of plasma membrane
- the membranes are part of specialized glial cells that wrap around axons of neurons in
PNS (schwann cells)

A depolarizing effect happens in the first node of ranvier and the schwann cells are myelinated
(which means that they are insulated: so they dont have open voltage gated channels) so it
seems as though the effect is just travelling from the first node to the second node (although
really the energy is conserved and transferred through the insulated myelination of the schwann
cells)

If you have a normally myelinated axon become non-myelinated (degeneration of a normally


myelinated axon)
Types of synapses:
1. electrical synapse:
- signals pass through gap junctions
- rapid conduction -> information can flow in both directions

2. chemical synapse: FIGURE 8.19


- when it is synapse between a neuron and an effector cell: neurotransmitter junction
Presynaptic cell: many vesicles -> contain neurotransmitter
(neurotransmitteres diffuse through the synaptic cell)
bind to receptors on postsynaptic cell membrane (results in changes in the postsynaptic cell)

KISS AND RUN (is the second way that the neurotransmitter can be resulted)
- the first is when the vesicles diffuses with the vesicle membrane and the presynaptic
membrane

Our cells are very good at keeping calcium levels very high in the extracellular fluid and up in
storage (but the influx of ions which causes the trigger of the neurotransmitter from the synaptic
vesicles)
- the synaptic vesicle kisses the docking protein (which changes conformations) and then
the vesicle runs away
- the vesicle interacts with the docking protein (the kiss) and when the

When the neurotransmitter is released it binds to the ion channel directly and influences an
influx/efflux of the ion (depending on what channel it binds to)

You have a presynaptic axon terminal releasing a neurotransmitter which diffuses across to the
postsynaptic membrane (the direct response is where the neurotransmitter binds to the ion
channel directly, and changes the shape (i.e. open or closes it)

Lecture 7

Q: When voltage gated Ca2+ channels in the axon terminal open:


a. the signal to open was axonal depolarization
b. Ca2+ enters the axon terminal
c. Ca2+ leaves the axon terminal
d. a and b
e. a and c
Cells are very good at keeping Ca outside the cell membrane, so when the channel opens,
calcium comes in and causes release of the neurotransmitter at the synapse

Neurotransmitter: 6 major types


3. amino acids: most abundant neurotransmitter in CNS
4. neuropeptides: peptide = small little protein, transcription and translation pathways so the
synthesis for neuropeptides are made in the rough ER where the rest of the cells proteins
are made, and then the vesicle travels down to the axon terminal and waiting for its
release at the synapse (to pass the signal along)
5. nucleotides can act as signalling molecules but there are receptors found in the CNS that
will respond to the release of ATP along the synaptic cleft
- the adenosine (nucleoside) can also act as a neurotransmitter
6. gases: kind of FYI

Neurotransmitter degradation:
Neurotransmitter inactivaton: FIG 8.19B

Action potential happens at the axon, it reaches the length of the axon terminus and releases the
synapse at the synaptic cleft (as long as there are neurotransmitters ???

1. neurotransmitters can be returned to axon terminals for reuse or transported into glial
cells
2. enzymes inactivate neurotransmitters
o the enzyme degrades the neurotransmitter so that it is no longer able to pass the
signal onto the post synaptic cell
3. neurotransmitter can diffuse out of the synaptic cleft
o if you get far enough away from the receptor then there is no response (it doesnt
just diffuse into the extracellular fluid but can also be diffused into the blood
vessel)
So if the neurotransmitter is taken away from the receptor, there is no interaction so the signal is
cut and that stops continuous firing

Smooth muscle might contract when exposed

Structure of autonomic division:


Ganglion: a cluster of cell bodies as part of the peripheral nervous system
In the diagram, for simplicity, there is only one shown but in reality you would have a lot
of cell bodies clustered together and its part of the autonomic system so its called the
autonomic ganglion
KNOW THE TERMS PRE-GANGLIONIC AND POST-GANGLIONIC

The short pre-ganglionic axons emerge from the spinal cords, and they have very short axons
(very short length) and the autonomic ganglion descend down the vertebrate column and that
reaches the post-ganglion neuron that is much longer and is able to reach the target cell

The pre-ganglionic (instead of the middle of the spinal cord) you have these exiting from the
brain stem (cranial nerves) and in the bottom of the spine section near the pelvic region
- FIG 11.5
o The target tissues for the sympathetic and the parasympathetic are the same

Neurotransmitters (FIG 11.6)


Describe that is happening at the different synapses in the sympathetic and parasympathetic,
what neurotransmitters are released and what the receptors involved do
BE COMFORTABLE WITH THESE TWO
PATHWAYS: MIDTERM QUESTION

Post ganglionic neurons are looked at when you are discussing the target tissue

FIG 11.7

Concept check queston on above diagram: it is a sympathetic pathway ^ (at the target tissue is
where you see the difference, if this was parasympathetic, you would see acetylcholine being
released)
Receptors:
when we take a look at the target tissue for the autonomic ganglia we find receptors
its not just a signalling molecule that gets released, the receptors are also important because
there are multiple types with various purposes

1. Adrenergic receptors are on the tissue cell (target tissue) that will respond to the
autonomic post ganglion sympathetic neurons
- BE FAMILIAR WITH THE BINDING DIFFERENCES BETWEEN EPINEPHRINE (E)
AND NOREPINEPHRINE (NE)

2. cholinergic reecptors the normal ligand is acetylcholine which stimulates both nicotinic
and muscarinic receptors
nicotinic receptors: the antagonist nicotine binds to this and causes the same type of
response
^ ACETYLCHOLINE IS COMMON IN BOTH
muscarinic: muscarinic as an antagonist causes the same response in the muscarinic
receptors

nicotinic receptors are always excitatory so it is a direct response because the receptor is
an ion channel so it opens up
muscarinic receptor is coupled with G proteins so it may cause different responses
whether it opens (excites) or closes (inhibits) the ion channels

Fig 11.9

Rest-and-digest: parasympathetic Fight-or-flight: sympathetic

Another word for epinephrine is adrenaline!


FIG 11.8 (ADRENAL MEDULLA)
Lecture 8

Q: T/F Somatic sensory neurons control skeletal muscle


a. true b. false (not sensory, somatic motor neurons!)

when the somatic motor neuron fires and moves down the length of an axon, it leads to firing of
an action potential inside the skeletal muscle (which causes contraction)
- so how we dont cause the skeletal muscle to contract is to not send a neuron; no neuron
fired means that no signal is delivered

Fig 11.10

skeletal muscle fibre : same as skeletal muscle cell (there are two indicated in the diagram)
each fibre is controlled by a single cell but a single somatic neuron is able to control multiple
cells (could be thousands)

the terminal bouton is where the somatic motor neuron attaches to the cell and spreads out a little
bit (it looks like when you are trying to spread out the jalepeno cream cheese)

motor end plate is a folded back and forth part of the skeletal muscle fibre
- nicotinic type ACh receptor channels (THE NICOTINIC ARE ION CHANNELS: which
becomes very important)

Neuromuscular junction is another term to describe the synpase between the somatic motor
neuron and the skeletal muscle fibre (divided into 3 different stages/parts)

an action potential arrives at the axon terminal, causing voltage gated Ca+ channels to open,
calcium entry (influx) triggers release of ACh by causing synaptic vesicles to fuse with the
presynaptic membrane and release ACh into the synaptic cleft
AChE is an enzyme that degrades ACh, when it degrades the ACh, there is no more
signal in the cleft so the signal cant be delivered

the channel remains closed in its normal state and waits for the signal to come in (ACh)
we need two ACh molecules to bind to the nicotinic receptors, which is an ion channel, so when
the channel opens (it allows both the passage of sodium and potassium)
- there is an unequal movement of sodium/potassium: more sodium ions are coming into
the cell than potassium can leave the cell
- the sudden influx of sodium will depolarize the cell and we get a signal/response
FIG 11.9

autonomic targets: smooth and cardiac muscles, some endocrine and exocrine glands, some
adipose tissue
a. parasympathetic pathway
b. sympathetic pathway
a and b share the same pre-ganglionic/post-ganglionic signal but when it hits the ganglion that is
where the difference occurs (between nicotinic vs muscarinic receptors)
c. adrenal sympathetic pathway
modified sympathetic ganglion (CHROMAFFIN CELL) that responds to a signal from a pre-
ganglion neuron, which is
without the chromaffin cells firing, the epinephrine would not be released

somatic: skeletal muscle

UNIT 3 MUSCLE:

smooth/cardiac: autonomic system,

Stores and hydrolyzes ATP, which leads to a contraction because of the proteins in the cells
when you cut/hydrolyze that ATP, heat is released which contributes to our maintenance as
homoeothermic animals

FIG 12.1
the skeletal muscle is attached to the bones/muscles of the body so when it contract is when we
find movement in the body
- the long cylindrical (skeletal muscle cell) has multiple nuclei (maybe even hundreds) and
it has a repeated light-dark banding pattern which is called as striations
smooth muscle is called smooth because there are no striations (no light and dark banding
patterns, they have the same proteins that cause contractions but there are no certain
arrangements of these tissues)

cardiac muscle only find in the heart, it has a very important job to provide a force of contraction
so that the heart can pump (the pumping increases the pressure of the blood inside the heart
which causes it to flow outside and throughout the body)
- highly branched and also the second of two types that is striated
think of it as her right and left hand as each different cardiac muscle cell, when you cross
your hands (not arms: hands) there is an interdigitated disk in the middle through which one
cell communicates with another cell (gap junction in the interdigitated disk so that the signals
pass through very rapidly)

A tendon is made up of connective tissue, lots and lots of extracellular matrix is found in
connective tissue (and there is lot of collagen present: in a tendon it is found in a cable like
form) FIG 3.13

FIG 12.3a
https://www.google.ca/search?q=skeletal+muscle+structure&safe=strict&espv=2&biw=
1440&bih=708&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiShbjsquDRAhVSPJA
KHZdaCsEQ_AUIBigB

epimysium: outer most layer of your skin if we peel that away, we find bundles (bundles of
cells called fascicles)
the fascicles are covered by a connective tissue layer called perimysium (the white-ish tissue
that wraps around the bundles of fibres: muscle fascicles)
- the perimysium is where the nerves and blood vessels are found

imagine the room: each one is a single muscle fibres (cell)


if you put your coat together, you are covered by a endomysium
and if you divide the class, half of it is one fascicle and the other half is another fascicle
the class (bundle of fascicles) are covered by the walls of the room (perimysium)
and the building is the epimysium (the outer most layer) !
- endomysium (surrounds a single muscle cell) FIG 12.3b

sarcolemma is the cell membrane of the skeletal muscle fibre


- myofibrils are the protein that are responsible for the contractile and elastic movement

the modified endoplasmic reticulum encircles the myofibrils

when you play with clay, if you poke a finger into it, and take it away you see a dent in the clay
(that hole is the T-tubule, now if you poke a hole in somewhere else, that is another T-tubule, but
the clay that is : example the division between the two sections of the classroom is the lumen,
and the first chairs on either side are the T-tubule)
- the second chair is the terminal cisterna which holds on too sequester/holding on to Ca2+
a triad is all the way from the second chair of one side of the class, the first chair on that side of
the class and the lumen in the middle (the aisle) and the first and second chair on the other side
of the class)
the combination of the terminal cisterna , T-tubule and lumen is called a triad

the function of T-tubule: the release of ca2+ from the SR helps in the contraction of the muscle
fibre

Lecture 9

Which of the follow are striated muscle?


a. Smooth b. cardiac c. skeletal d. a and c e. b and c

Myofibril: long cylindrical structure found inside skeletal muscle fibre, so when you focus on
one individual myofibril, you find proteins: actin and myosin
- When these proteins come together, there is a contraction in that muscle
- The actin/myosin have to have some way to be controlled/regulated
- We have to understand how actin/myosin are organized into fibrils, and how they cause
the muscle to undergo contractions

Regulatory proteins: regulate whether or not a contraction should be allowed to happen inside a
myofibril (tropomyosin and troponin)

Accessory proteins: help organize the myofibril

What causes striations?


Skeletal muscle fibres under the microscope have a very organized unitof proteins which gives
rise to a light-dark-light-dark banding patterns, called striations
- Names were given to the repeated structure of the organization of the proteins when
witnessed under the microscope:
KNOW THESE: be familiar with the various structure in the repeated unit

Z-line (disk)
I-band (given name according to how they look under the microscope and how light reflects,
so the I band is the light band in the light-dark banding pattern)
A-band (dark: this is dark because there is too much protein that is scattered to allow light to
pass through uniformly so it looks darker)
- There is a slight area within the A band that is a little lighter (not as light as the I band)
known as a H zone
Course notes: page 53
The Z-line passes through an area that is pretty light under the microscope, that lighter area is
called the I-band

The thicker lines are the dark part of the light-dark banding, called the A band
- The repetition of the structure again and again is called the sarcomere
Figure 12.3(?) b and d

The two main contractile proteins are organized in a way that gives rise to the striations, in not
just skeletal muscles but also cardiac muscles

Make a fist, and hold your arm out at an angle (similar to the picture on page 54)
- The fist is the myosin heads, which extends to the outer part of the thick filaments
- And your bicep area is the tail region, which orient towards the middle of the thick
filaments
- From your wrist to your elbow is the hinge region which allows for very flexible
movement of the heads
Now if you hold both arms out (like a titanic pose) your body becomes the M line and the tails
would have orient themselves towards the middle and attach to the M-line

Binding sites:
- Myosin binding site is ATP
- Actin binding site is (?)
Actin is the only protein (very important) found within the thin filament, it is a contractile
protein which forms the basis of the thin filament but the regulatory proteins help to complete the
thin filament
Fig 12.3f

Cross bridge (KNOW THIS)


The myosin heads interact directly with actin filaments, these interactions are called cross
bridges

Fig 12.8

I-band
The Z-disk goes right in the middle of the I-band so it divides the I-band in two parts, where one
part interacts with the sarcomere and the other part of the same I band interacts with the
neighbouring sarcomere

The center part of the A band (H-band) is where you would find think filaments only

The tails orient themselves towards the M-line


The outer edge of the A band is the only part where you find the overlap between thick and thin
filaments ,
single thin filament is always surrounded by three thick filaments within the particular structure

Titin very large proteins: Fig 12.6

Titin: helps relax the force by providing elasticity


Nebulin: the tropomyosin is like a rope so there isnt much you can work around to make sure
the globular actins line up along the thin filament for good organization

An indentation (like the align in the middle of the room) in the sarcolemma is called T-tubules
(tranverse tubules)
- They have a job: they conduct action potentials (getting the action potential into the
skeletal muscle fibres)

Mechanisms of muscle contraction


- Early theories suggested that muscles were made of components (molecules) that shorten
when activated and stretch at rest

Researchers knew that myosin shortens when heated (steak) so they assumed it was the active
component
- Steak is flesh (skeletal muscle) too much heat will cause the steak to shrink, because
myosin shrinks when heated which was the early theory

It wasnt until 1954 that two researchers questioned that if the theory were true that you would
see changes in the A-band because that is where you find the myosin, but they realized that the
A-band wasnt changing in length at all
- So what other explanations did they have?
They proposed the sliding filament theory (which comprises of the thin and thick filaments)
- At rest you have the conformation of the A-band and I-band in the sarcomere
arrangement and at the outer edge of the A band is an optimal degree of overlap of the A
and I band with the heads of the myosin pointed towards the thick filaments
- The myosin proteins pull the actin thin filaments closer towards the M-line which brings
the Z-disk closer together
- There is no change in the size of the thin or thick filament, they are just sliding closer to
the M line
the myosin can pivot because of the hinge region

Cross bridge cycling: what happens when a muscle undergoes contractions which causes sliding
filaments to slide past one another (we called it cross bridge because that is where actin and
myosin come together)

Power stroke: now myosin has pulled actin along with it as it pivots back to the 45-degree angle

Relaxed muscles are mostly in step 2 (myosin heads at 90-degree and weakly bound to an actin
molecule)
During contraction the myosin heads dont move simultaneously (usually 50% moving, 50% are
attached)

What would happen if all the cross bridges released together?


- The thin filaments would slide back to where they were
- Thin filaments would slip back into their orginal positions and the contraction would not
occur
- Imagine you are play tug of war, the hands of your team members are myosin heads so
you would not want all the hands to give up at the same time because then the rope would
return to its original position
- Remember when you play tug of war, you play hand over hand so one hand is more
predominantly pulling than the other you move hand over hand and thats how the
myosin heads move and pull (if you were to pull with both hands and release both hands
(in order to move them forward) you would end up letting go of the rope completely
- So one hand at a time

Midterm review:

The type of tissue provides structural support and barriers: connective tissue
Epithelial: protection and exchange of materials

The maintenance of a relatively stable internal environment is known as homeostasis

Which of the following allows direct cell to cell communication? Gap junctions

Neurons that lie entirely within the CNS are called interneurons

Which of the following glial cells has extensions that contact blood vessels in the brain?
Astrocytes
Microglia: look for damage tissue
Ependymal cells: lining the cavitity separating the CNS
Satellite cells

A collection of neuronal soma outside the CNS is called a ganglion and within the CNS is called
a nucleus

Concentration gradient between a cell membrane is more K ions inside and more Na ions outside

The value of the resting membrane potential is -70

The resting membrane potential depends on each item below expect:


Greater membrane permeability to anions rather than cations
Other options:
(concentration of Na inons)
(greater permeability of plasma membrane to k ions)
(greater leaky channels of K ions)

a neuron under the influence of a neurotransmitter that opens k channels will be less likely to
cause an action potential

a threshold stimulus immediately fully opens voltage-gated sodium channels

influx of na ions in one area of an unmyelinated axon initiates which of the following events?
AP in that area and depolize area to threshold

Action potential progration in myelinated axons is known as salutatory conduction


Which of the following differentiates skeletal muscle from both cardiac and smooth muscle?
Multinucleated fibers
(both are striated)
(all muscle can generate force)

which of the following connective tissue sheathes directly cover skeletal muscle fascicles?
Perimysium

Terminal cisternae sequester Ca ions

Which of the following are contractile proteins in muscle? Actin and myosin

What triggers myosin to release from actin in the cross bridge cycle? Binding of ATP

Lecture 10 MIDTERM
Lecture 11 Missed Class
Lecture 12
Which of the following are energy sources for skeletal muscle contraction?
a. Oxidative metabolism
b. Glycolysis
c. Creatine phosphate
d. b and c
e. a b and c

Oxidative vs glycolytic: the primary production of ATP


- Red coloration is accumulation of protein (myoglobin) found in the oxidative fibres
- Myoglobin contains a heme- (like hemoglobin) group that is able to bind reversibly to
oxygen, and store oxygen within the cells that are for oxidative fibre metabolism type
- The rate of the diffusion of gases is limited by the distance, so the farther the distance, the
lower the rate of diffusion, which is why the oxidative fibres tend to be smaller whereas
the glycolytic fibres are more wider (because the rate of diffusion doesnt have to be too
small)

How quickly can a myosin protein hydrolyze/cut an ATP fibre?


- Fast twitch fibre: split ATP fibre, because they are able to do that, they are able to go
through a cross bridge cycle
- When that is able to occur very quickly, you are able to have the sarcomere undergo
contractions/movements at a quicker pace
- The slower fibres have an isoform (version of the protein) which is different so it is not
able to hydrolyze as fast as possible
No tension originally developed, but when the myosin is going through the cross bridge cycle
(rubbing, pulling, grabbing the thin filaments to slide past one another), tension increases
because that is the contraction phase

- The relaxation phase is when the myosin is no longer to interact with the actin

There is a delay between when we get a stimulus and actually see a contraction latent period
- Our action potential starts on a motor end plate

Which type of muscle has a higher rate of Ca removal from the cytosol?
- FAST TWITCH MUSCLES (WHY: KNOW WHY)

A single twitch is a single relaxation contraction cycle

The outer edges of the A band is where the myosin and actin (thin and thick filaments) and how
much they overlap is proportional to the amount of force generated
- For a single skeletal muscle fibre (a single sarcomere) that is an optimal overlap to
generate a certain amount of force

A single twitch does not represent the maximum force that a single muscle fibre can develop
- The stimulation always comes from action potentials, that arose from the stimulus of
somatic motor neurons
- So the rapid rate at which somatic motor neurons stimulate action potentials (which in
turn stimulate muscles: the force that is generated is higher)
CONCEPT KNOWN AS SUMMATION

FIG 12.16

When a cell keeps repeatedly getting stimulated but not quick enough then you see three
different twitches
- When the stimulus summate (because they happen close enough in time to cause the cell
to experience a greater force before returning to rest
- If the stimulation happens before the cycle has completely fully relaxed, the cell will
undergo a greater force of contraction, a cell will continue to be stimulated until the
maximum tension that the muscles can feel has been reached

Tetanus: when a skeletal muscle cell reaches its maximum force (tension) of contraction

Unfused tetanus is when you have reached the maximum amount of tension, but there are
chances when the cell is ever so slightly allowed to relax before contracting again
- The period where the tension is building up to the maximum amount is called summation
- So the tetanus is when the max tension has been achieved, summation is the period
leading up to that
The cell gets hit with a rate of stimulation that was so fast that it reached the maximum tension,
and at that point too, it keeps going (horizontally) maintaining the maximum tension, until
fatigue causes the muscle to lose tension despite continuing stimuli

Fig 12.17

Which will be recruited first oxidative or glycolytic fibres? Oxidative

We have more motor units for fine movements because we wanna be able to tweak and refine
what contractions are happening

Recall skeletal muscles are attached to the bones of the movement, but there are different types
of movements of the skeletal muscle which results in different contractions
- There are two main types: isotonoic and isometric

Lecture 13
A single motor unit consists of
a. Somatic motor neuron
b. Muscle fibres of different types
c. Muscle fibres of the same type
d. a and b
e. a and c

To hold the arm stationary at 90 degrees, the rotational force created by the contracting biceps
must exactly oppose the downward rotation created by the forearms weight
Rot force up = rot force down
Biceps force x 5 cm = 2kg x 15 cm
Biceps force = 30 kg*cm / 5 cm
= 6 kg

Sphincter: smooth muscles that are organized in a ring like structure that are able to close/open
an opening allowing passage when they relax or contract

The small intensitines contract have a circular arrangement around the contraction

Multi unit arrangement


All the cells get stimulated thanks to the minority of cells that start interacting due to the original
stimulus

Just before labour (pregnancy) there is a remodelling of the cell from a multi unit type to a single
unit type, this happens because it is believed so that the contractions are happening together as
one unit rather than one part of the uterus contracting while the other isnt

Contracts more slowly and for longer periods of time than skeletal/cardiac muscle
What would happen if your bladder were lined with muscle organized in sarcomeres?
- When the balloon fills up, as it fills up with the liquid that is transferred from the kidneys,
if it were organized in sarcomeres, you wouldnt get any tension developed beause the
thin filaments cant be grabbed on by the myosin heads, so since it is unable to grab there
arent that many contractions happening

Ca coming from outside the cell causes a release of the intracellular calcium storage causing a
higher level of intracellular calcium
- Calmodium binds to the calcium (inside the cytosol) and forms a calcium calmodulin
complex which activates an enzyme known as myosin light chain kinase (MLCK)
- The job of this protein is to add a phosphate group onto something (kinase :
phosphorylation addition)

The role of myosin being regulated via phosphorylation in smooth muscle is VERY different
from actin being regulated through troponin/tropomyosin in skeletal muscle

What would happen to contraction if you put a smooth muscle cell in Ca2+ free solution?
- You wouldnt get any contractions
- What triggers contraction is the influx of Ca2+ from the extracellular environment, so
there isnt any calcium to come into the cell initially which causes a lack of contraction

Calcium can be pumped out of the cell through a sodium calcium ATP,
Or you can use an influx of sodium coupled with an efflux of calcium
Either way calcium has to get out of the cell
Which causes a break up in the calcium calmodulin complex, which inactivates MLCK

There is another protein that is always active in the background, known as myosin light chain
phosphatase, which take the phosphates away from the myosin heads so it goes from activated to
inactivated

Lecture 14 Missed Class


Lecture 15
Q: The cardiovascular system
a. Assists removal of wastes
b. Distributes respiratory gases
c. Functions in transports of hormones
d. a and b
e. a b c

Figure 15.1 (Oxygen poor blood: represented in blood coloration)


- When this blood leaves the heart, it moves towards the arteries
As the blood drops to the heart, it has too little pressure to travel back which is why we need two
pumps in a series.

The tip (of a cone) when you hold an ice cream cone is known as an apecs
- The heart also has a conical shape, with a slight tilt, so it also has its own apecs, and the
larger in diameter (the top part: where the ice cream goes) is known as the base
- So the superior part of the heart where the blood vessels attach is known as the base
- The inferior portion of the heart is known as the apecs

The heart is surrounded by a double membrane stack (The pericardium)


- The inner membrane rests exactly right on top of the heart
- Whereas the outer membrane is seen attached to retractors that seems to be pulled away
from the inner membrane (leaving a black space in the diagram) but in real life there isnt
any space between the two membranes

The coronary arteries can get blocked, depending on where the blockage occurs, the amount of
damage done to the muscular system, creates a shortage in blood suppy to the heart which causes
a heart attack
- BUT THE IDEA TO TAKE HOME IS: the coronary artery has its own set of
arteries/vessels that supply blood to the sac

When you see hearts in diagrams, its like you are looking at the heart of someone else who is
standing directly in front of you, facing you.

Figure 14.5

The tricuspid is on the right side (the bicuspid is on the left)


- These valves have specialized cords that connect the AV valves to the inner lining of the
ventricle
- The cords make sure that the valves dont end up going back into the atrium (preventing
backflow of blood)

Prevents the backflow of blood that has left a ventricle and entered into the artery

Figure 14.7

During ventricular contraction, the AV valves remain closed to prevent blood flow backward
into the atria
(The bicuspid or the mitral valve shuts)

When the ventricle is relaxed (the time of the cycle when it is filling up with blood), we want the
blood to flow from the major blood vessels that are brining blood to the heart, past the atria and
into the ventricles
(The blood from the pulmonary veins)
The semilunar valves prevent blood that has entered the arteries from flowing back into the
ventricles during ventricular relaxation
The spiral arrangement of the cardiac muscle allows the maximization of the blood (like a towel
that is wet, when you want to dry it, you take both the ends and twist it, instead of the just
smushing the towel together)
- This twist motion (isnt exactly what happens in the heart but) allows the spiral shaped
cardiac muscles to deliver the maximum amount of blood during contraction

Be familiar with both auto rhythmic cell and contractile cell because action potentials in both of
these look very different!

The time period for the action potential in pace maker cells (depending on how many times it
beats per minute which is individual to each and every one of us)

EVERY CARDIAC MUSCLE CELL (PACEMAKER OR CONTRACTILE ARE


CONNECTED TO THE GAP JUNCTIONS)
- The fastest cells in the SA node are what drive the heart rate

Figure 14.19

Lecture 16
Q: The unstable membrane potential observed in pacemaker cells is due to:
a. Na+ efflux / K+ efflux
b. Na+ influx / K+ efflux
c. Na+ influx / K+ influx
d. None of the above

If = funny ion channels.

Coordination of contraction

1% of cardiac muscles cells are not contractile


- Involved in electrical excitation of heart > conducting system
- Initiate heart beat
- Allow it to spread rapidly throughout heart
- Connected to other cardiac cells via gap junctions

The heart contracts in a very coordinated way to effectively pump blood out of the heart
FIGURE 14.13

Pathway of conduction:
Pacemaker cells in the sino-atrial (SA) node generate action potential
The pathway always start with the fastest cells in the conducting system, which are in the SA
node because of their funny ion channels, they are able to spontaneously generate action
potentials which then spreads to neighbouring cells through gap junctions

1. Internodal (in between the SA and the AV node) pathway connects the SA node to the
atrioventricular (AV) node in the floor of the right atrium
2. AV node action potentials enter more fibres called the BUNDLE OF HIS (AV Bundle)
The bundle divides into left and right bundle branches
o PURKINJE FIBRES (rapid electrical signalling of action potentials)
Spread out into contractile cells (of the ventricles)

Figure 14.14

The ventricular septum is the wall that divides the light and right ventricle

Events in conduction of an AP
1. AP fired from SA node
2. Spreads to adjacent cells > via gap junctions
3. Rapid spread through cells of internodal pathway
a. Spread is slower through contractile cells of atrium (than the pacemaker cells
found in the internodal pathway) WHY?
ANS: Resistance, contractile cells are supposed to contract, so the flow of the charge
that hits the chalk material of the contractile cells required to contract, there is a delay
because of high organization and make-up of contractile cells

4. Signals passed through AV node only at AV junction -> layer of fibrous material acts as
an insulator prevents electrical signals from atrium -> ventricle
a. AV node only pathway for AP
5. Signal is slightly delayed by AV node: WHY? To ensure atrial contraction is over
6. Signal is carried to bottom of the heart (APEX) through Bundle of His
Why is it necessary to conduct signals only through AV node & bundle of his?
[Like a tube of hand cream, if you want the cream to come out, you press from the bottom all the
way to the top so in order to maximize the blood flow, the AV node at the bottom of the right
atrium leading to the bundle of his is required to carry the signal all the way down to the apex
and to the purkinje fibres]
So that signal for contraction initiates at the bottom of the heart
This ensures the contraction drives the blood up since it leaves the heart at the top

Abnormal heart rhythm: arrhythmia can develop


a. When another part of the heart takes over as pacemaker
b. When the SA node develops an abnormal rate/ar-rhythm
c. When the normal conduction pathway is interrupted

Bradycardia: slow heartbeat > less than 60 bpm: fatigue, dizziness, light-headedness, fainting
(The normal heart rate is somewhere between 60 100)
May occur as a result of physical conditioning (e.g. endurance in runners)
Serious cases result from blockages in conducting pathways of heart
Treatment: electronic pacemaker
(Unable to conduct enough blood to various regions of the body for proper functioning)

Tachycardia/Tachyarrhythmia: rapid heart beat > more than 100 bpm


Palpitations, rapid heart beat
Ventricular fibrillation (V-fib)
Disorganized contraction
Ventricle quivers > heart cannot pump any blood
Collapse and sudden death follows unless medical help is provided immediately
Treatment: can be converted into normal rhythm with electrical shock (defibrillator)

Atrial fibrillation
Atria quiver instead of beating effectively
Blood isnt pumped out completely when heart beats
Blood pools and clots : if lodged in artery in brain : stroke (coronary arterties?)
15% of strokes occur in people with A-fib
Treatment: atrial contraction is unimp. for cardiac function except during strenuous
exercise therefore treated with aspirin and warfarin: interfere with blood clotting, reduces
risk of stroke

Electrocardiogram: use 3 leads to make Einthovens triangle


- Clinically use 12 ECG leads -> given information about different regions of the heart
Figure 14.15
Each and every lead is like a camera angle, that gives you shot of the heart to depict what
happens (Lead consists of two electrodes, one positive and one negative)
- Electrodes are attached to the skin surface
FIGURE 14.15D
When we see deflections either above or below the baseline, we are seeing

Components of ECG:
1. Waves
Deflections above or below baseline
Electrical events
3 major waves:
a. P wave: depolarization of atria
b. QRS complex: ventricular depolarization
c. T wave: repolarization of ventricles

The ECG diagnostic tool

Cardiac cycle
Two phases:
Systole: contraction
Diastole: relaxation
Lecture 17
Q: In the cardiac cycle, relaxation is called
a. Systole
b. Diastole

Possible questions on systole/diastole: ventricular and atrial

Factors influencing heart rate:

Parasympathetic and sympathetic are direct via the nerves versus plasma epinephrine
reinforces

The stretch of the sarcomere gives more binding sites for the myosin (but there is limited
elasticity meaning that you cant stretch too much)

The walls of blood vessels can be made up of multiple layers,


Important to note which type of blood vessels contain which type of layers (in the walls)
because not all type of blood vessels has all type of layers

- Blood vessels are tubes that are surrounded by walls (each with different layers)
- But the center of the tube is the lumen (the inner central cavity)

B/D elastic and fibrous connective tissue are each individual layers of connective tissues
The elastic is called elastic because it has the ability to stretch and then recoil

When the vascular smooth muscle layer contracts, it takes the lumen and the diameter of the
lumen shortens (vasoconstriction)

There are five types of blood vessels make a note of the different type of wall found in each
a. Artery (carry blood away from the heart) so it must be able to withstand blood at its
highest pressure (when the blood is being pushed out of the heart through the pumping
motion)
ALL FOUR LAYERS
b. The arteries start to branch as it moves away and away from the heart and the pressure
in the blood starts to decrease (arteriole) are able to regulate the flow of blood through
them thus they are able to dilate/constrict in order to direct the blood flow
Smooth muscle lining and endothelial cell lining (what faces the lumen)
c. Gas exchange happens in capillary beds but for adequate amount of exchange to
happen you must have a small diameter between the different cells
Thus the capillary is very small, and made up of
Layer of endothelial cells
Diffusion and gas exchange are correlated to distance so the further away the gas exchange is
going to have to travel, the less diffusion you will have thus it is important that capillaries are
small
d. Venule: small veins that branch out from the capillaries
inner most lining of endothelial cells and fibrous connective tissue lining
e. Vein blood is being carried at a very low pressure but we want the blood to flow nicely
thus
All FOUR LAYERS

Lecture 18
Pressure always decreases by friction

Adjustments are made by changing r the radius of the blood vessels


- Arteriole (peripheral) are found in the systemic ___ and they are very good at regulating
the flow and resistance of the blood, so there is a really good shift in the flow of blood
at the arteriole level

With regards to pressure gradient and resistance, we can understand the flow of blood as it
flows through our network of blood vessel (F directly proportional to pressure gradient (from
high to low, so at the exit and entrance of the heart, respectively)
- Setting up that pressure gradient will cause flow to occur
- Inversely proportional to radius

(1) Systolic and (2) diastolic pressure:


1. The time when the heart is contracting
2. The time when the heart muscles are relaxing
As the pressure gauge increases, the pressure of the cuff increases, so that when it squeezes on
the outer part of your arm, it is hopefully squeezing that artery enough to momentarily block
any blood flow through that artery
- As you release, VERY SLOWLY, the air from the cuff, you have to listen very carefully
- Now suddenly, the artery that had been blocked is now being open so you get a very
narrow passage through which blood is allowed to pass
- When you dont hear the turbulent sounds at all, you have your diastolic pressure

Figure 15.6: Changes in pressure that is recorded by tracking in different areas of systemic
circulation of the blood in the cardiac system
Low pressure when it relaxes, high pressure when it contracts

Be familiar with the MAP formula

If we change cardiac output, we will be able to influence or change in mean arterial pressure
(MAP)
- Either heart rate or stroke volume will influence cardiac output

Baroreceptors: pressure receptors (barometer: the pressure of the atmosphere) baro =


pressure
Make sure the pressure is adequate enough so that it can undergo the journey to supply
oxygenated blood to our very oxygen dependent brain
- Mechanoreceptors: some sort of physical force that is applied to a cell to activate the
initial signal in a cell

Figure 15.14

What is blood?
Plasma: fluid portion of the blood
Red blood cells -> erythrocytes
- The job of the hemoglobin is to be able to bind reversibly to gases, mostly oxygen and
carbon dioxide for transport

White blood cells -> leukocytes


- Lymphocytes are a type of white blood cell, but leukocytes means white bloods cells
(all inclusive)
- If you take a sample of the blood, separate the white blood cells and analyze them, you
discover that anything that is a foreign identity (no matter what), the WBC will ingest it
through phagocytosis
o Basophils are immature mast cells, allergies are mast cells (overreacting to
something that shouldnt be considered harmful to our body)
Never let monkeys eat bananas (NLMEB): Neutrophils, lymphocytes, monocytes, eosinophils,
and basophils are our different types of leukocytes

Platelets - thrombocytes, involved in blood cotting


- Derived from megakaryocytes: pinch off and have no nucleus

Pinched off little extensions that (without stimulus) are inactive, thus always found in the blood
RBC need adequate amount of hemoglobin (it is made up of four protein chains (subunits))
Called globins, because they are globular (round, spherical) proteins rather than linear protein
chains

Why do we see a different form of foetal (fetus) hemoglobin and the maternal hemoglobin?
- The foetal hemoglobin needs to pull more oxygen away from the maternal, so with
better binding abilities, it is better able to scoop the oxygen away as the mothers
hemoglobin is their only way of attaining oxygen
- Whereas a mother gains oxygen when she births in (therefore, the babies hemoglobin
needs to be stronger than the mothers so that the oxygen from the mothers is
efficiently transported to the babies blood)

Figure 16.6

We can explain the saturation of hemoglobin using a hemoglobin oxygen saturation curve
Capital P represents the partial pressure of the gas, in this case oxygen which describes the
amount of gas that we will find in the system

Lecture 19
Q: Platelets are also known as which of the following:
a. Erythrocytes
b. Megakaryocytes
c. Leukocytes
d. Thrombocytes
e. None of the above

Figure 16.2

Figure 16.4c

The mechanism by which we form thrombocytes

Figure 16.7b/c
As the damage occurs, platelets activate and group together to form something called a
platelet plug

The thrombocyte goes from a smooth looking surface to a activated platelet form

When EPO enters the bone marrow, it acts on the stem cells and causes the
maturation/formation of RBC (red blood cells)

Figure 16.9
Know the common pathway: where the instrinsic and the extrinsic meet to form the blood clot

Areas in the lungs that are geared towards gas exchange are known as alveoli

The bronchi branch further and further into bronchioles, that branch further into terminal
bronchioles

Figure 17.2

Lecture 20
Q: Which of the following are components of the respiratory system?
a. Exchange surface
b. Conducting system
c. Pumping system
d. a and c
e. a b and c

The thickness of the ventricular walls is different between the contractions on the left side of
the heart vs the right side of the heart
- eventually the pressure develops in the right chamber, which leads to lower pressure in
the blood as it leaves the heart
- the blood should have enough pressure to defy gravity, flow all the way around the
body and return back to the heart

Boyles law: pressure is inversely related to volume

Figure 17.5

This orange blob is the protein channel known as the NKCC channel (because it transport one
sodium, one potassium, and 2 chlorides)

If the cilia are paralyzed, they cant move and cant engage in the movement in the respiratory
tract

If the chlorine channel doesnt work due to a mutation, where it is unable to pump chloride, if
chloride cant get pumped out, sodium wont follow, so then water wont follow

When we expand the chest, we increase the volume of the chest, so the pressure within the
chest decreases and gases flow from an area of high pressure to an area of low pressure

If there is a break in one of the way pleural membranes, atmospheric pressure gets introduced
and the individual suffers from collapsed lungs

Compliance, resistance and elastis are factors that impact breathing

When the lungs are stretched, it allows the alveolar cells to release surfactants easier

Fetal development puts lung development on hold because really the lungs arent needed until
the baby comes out and takes its first breathe, so when an individual is born premature the
type 2 alveolar cells arent functioning at its full capacity (if born more than 6-8 weeks
prematurely)
The cells arent mature enough to produce an adequate amount of surfactants so the lungs
themselves dont have the ability to be compliant, which causes difficulty in breathing

A normal lung is like a balloon, it has elastance so that when you blow up a balloon, it expands
and then when you let it go, it goes back to normal (air is being pushed out by itself)
- in an emphysema lung, imagine a paper ball
- you blow it up and it expands but then when you let it go, the air doesnt get pushed out
so you have to forcefully squish the bag with your hands to get the air out (i.e. breathing
is forced)

FIGURE 17.7
Lecture 21 Missed Class

Lecture 22
Q: The diaphragm can initiate contractions spontaneously
a. true
b. false
Venous PCO2 increases, but arterial doesnt

Arterial PCO2 set by alveolar PCO2

Venous PO2 decreases but arterial doesnt

Chapter 17 and Chapter 18 Tonights Quiz

When you suffer from an autoimmune disorder, it is because your body is recognizing foreign
particles that are actually not that dangerous but the body perceives it to be, causing a greater
reaction than that would be expected

Bacteria can enter the body, remember what protects the inside of our bodies from the outside
world is skin, but even inside our body, our body is protected because the lumen of the multiple
pathways that you can take to the inside of your body is separated from the rest of your body
(i.e. the respiratory system lumen (airways), the oral system lumen (digestive tract))
- The key message to take is that bacteria can survive in intracellular and extracellular
conditions
- Antibiotics only target bacterial cells
- You can not treat a viral infection using an antibiotic

A course of antibiotics always needs to be finished because you need to ensure that there are
no survivors at the end, because otherwise you might develop strains of resistant bacteria to
that antibiotic, which down the road leads to problems because then you are unable to handle
it with just an antibiotic

There is a net movement of fluid from the plasma of the blood into the capillary and out into
the tissues (?)

Lymphatic capillaries pick up the extra little bit of fluid and ultimately (through a long path) get
right back to venous circulation, where the fluid returns back to the plasma of the blood
- The flow of the lymphatic is through the movement of your body (there is no pressure
gradient that supports the circulation)

Lymph nodes : FIGURE 24.3


The green lines drawn are lymphatic vessels (the movement of these body parts causes the
lymphatic fluid to circulate within these vessels)

With regards to immune system function, here is the job of the bone marrow and thymus:

1. Bone marrow: there are strategic parts in the human body where the bone marror is
activated (hemapoiesis: collection of all types of blood cells)
- RBC, WBC, and platelets produced here
- There is a specific type of WBC called B-cells that matures in the bone marrow
- When the T cells are produced in the bone marrow, they are still considered immature
- So they travel to thymus
2. The T cells reach the thymus and mature so that they are able to progress and continue
their function (which will not happen until the maturation process is complete)

Primary organs are those that produce T cells and B cells and help to undergo maturation (bring
it to finish)
- Secondary organs job is to help the cells carry out their function

Never Let Monkeys Eat Bananas Helps you recognize different types of RBC

Lecture 23
Q: All white blood cells are called lymphocytes
a. True
b. False

Lymphocytes are a type of white blood cells, with multiple types of lymphocytes!

B lymphocytes (B cells)
- Mature in the bone marrow (Bone marror: thus B cells)

T lymphocytes (like every other cell in the blood) is produced in the bone marrow, but it
undergoes a maturation process in the thymus (THUS T cells)

The Y shaped proteins (the arms are what recognize the antigen) and the stem stays of the B
cell, known as the B cell receptor

If the antigen is being presented on the surface of the cell (via the MCH proteins)

MCH proteins are expressed on the surface of the cell and will show antigens
- Self and non-self
Class 1 (found on all nucleated cells)
- A cell in your body that doesnt have a nucleus: blood cell (thus these dont represent
Class 1 MHCs)
Class 2 (found on APCs)
Pretend you have an epithelial cell in your nasal passage that gets affected by the viral cell,
the epithelial cells will take some of the viral proteins and via the MCH proteins will display
the antigens to the surface of the cell (the non-self antigens: antigens that are displayed on
the surface of a cell but are not belonging to the cell)
o This sends a red signal to the bodys immune system because the antigen
detected is a foreign material (certain MHC proteins in the body: a large amount
are quickly able to detect the smallest of foreign bodies)

Two main types of T cells:


- Kills and expresses appropriate Ag

Back to the epithelial analogy: as a viral infected cell, this cell will try to divide and repopulate,
but it has a Class 1 MHC that it will use to display the viral antigens on the surface of the cells,
the cell that can respond to that viral antigen (through the immune system communication
processes) and the killer T cell will kill the target (viral-infected) epithelial cell through
programmed cell death (apoptosis)

Antibodies : bind to antigen (Ag) as a signal

Cytokines : affect growth or activity of other cells

Innate and acquired (adaptive and specific) immunity

Humoral immunity (antibodies Ab)

The skin isnt the only part of your body that is in contact with the external body

Phagocytes: extravasion/diapedesis
- Imagine the desk as being the capillary layer in the endothelial cells in the tissues of our
bodies, but as a the phagocyte you are stuck in that lumen/layer but you cant just bust
through the cell, the phagocytes attach to the lumen (the desk) and just roll along the
desk towards an area that has an attractive force towards the other cells (it initiates
junctions and enters the tissues of the body)
- This process happens because of the chemoattrant damage to the phagocytes (kinda
like Starbucks to the customer, the smell that attracts)

Some pathogens are tricky, and cannot be recognized as being a foreign entity by the
phagocytes
Tagging: opsonization
Protein to do it: opsonin
The immune system is smarter though so the protein attaches to the pathogens and flags/tags
it so that it becomes visible to the phagocyte

Figure 24.6

Phagocytosis:
Form a phagolysosome

NK dont have specific receptors: like B and T cells

Inteferons: interfere with viral replication

Acts on endothelial cells lining blood vessels -> loosens junctions b/n cells

Compliment proteins are very large group of proteins: there is a sequential, one-after-the-other
proteiolysis (activation of the protein)
- Membrane Attack Complex (MAC) insert themselves into the membrane of a pathogen
and forms a hole so that water and ions (Na, Cl, K) causing the cell to swell until it lysis

THE MAC ATTACK