HUMAN EMBRYOLOGY

Dr. Qaiser Inayat

Associate Professor
Department of Anatomy
Khyber Medical College
Peshawar
 GAMETOGENESIS
 It is the process of formation of specialized generative
cells called gametes.
 In males, it is Spermatogenesis
 Process of producing sperm
 Occurs in seminiferous tubules of the testes
 In females, it is Oogenesis
 Process of producing oocytes
 Occurs in ovaries
 SPERMATOGENESIS
 It is the entire sequence of
events by which the primitive
germ cells-spermatogonia are
transformed into mature
gametes called spermatozoa.
 The process begins at puberty
(13-15 years) and continues into
old age.
 The process takes place in the
testes which are kept outside
the body hanging in a pouch of
skin called the scrotum. The
scrotum keeps the testicles 3°C
cooler than the body’s
temperature to keep the sperms
viable.
TESTES
 Brain-Testicular Axis
 Testicular regulation involves three sets of hormones:
 GnRH - gonadotropin-releasing hormone
 Secreted by hypothalamus
 Stimulates secretion of anterior pituitary secretion hormones (FSH/LH)

 FSH and LH - Follicle stimulating hormone and leuteinizing hormone

 LH act as Interstitial Cell Stimulating Hormone
 Secreted by anterior pituitary
 Directly stimulate the testes
 FSH - stimulates formation of ABP (androgen binding protein) by nurse cells
 LH - stimulates interstitial cells to secrete testosterone
 Testosterone
 Secreted by cells of Leydig (Interstitial cells of seminiferous tubules)
 Exert negative feedback on hypothalamic and ant. pituitary hormones
 Stimulates spermatogenesis by binding to ABP and development of
secondary sex characteristics
Hormonal Regulation of
Testicular Function
 Feedback inhibition on the
hypothalamus and
pituitary results from:
 Rising levels of
testosterone
 Increased inhibin

Figure 27.10
 Testosterone
 Most from interstitial cells of testes with small amounts from adrenal
glands and sustentacular cells
 Causes enlargement and differentiation of male genitals and reproductive
duct system
 Necessary for sperm cell formation
 Required for descent of testes
 Hair growth on certain parts of the body
 Skin is rougher and coarser
 Quantity of melanin increases
 Increases rate of secretion of sebaceous glands
 Hypertrophy of larynx
 Increases metabolic rate
 Increases red blood cell count
 Increases protein synthesis, rapid bone growth
 Causes closure of epiphyseal plates
Mechanism and Effects of
Testosterone Activity
 Testosterone is synthesized from cholesterol
 It must be transformed to exert its effects on
some target cells
 Prostate – it is converted into dihydrotestosterone
(DHT) before it can bind within the nucleus
 Requires the enzyme 5alpha-reductase
 Neurons – it is converted into estrogen to bring
about stimulatory effects
 Reqires the enzyme aromatase
 Testosterone targets all accessory organs and its
deficiency causes these organs to atrophy
 Accessory Glands
 Seminal vesicles
 Empty into ejaculatory duct
 Produce about 60% of semen
 Secretion contains fibrinogen
 High pH
 Prostate gland
 Produces about 30% of semen
 Thin, milky secretion, high pH
 Contain clotting factors, and fibrinolysin
 Bulbourethral glands
 Contribute about 5% to semen
 Mucous secretion. Just before ejaculation
 Helps neutralize pH of female vagina
 Semen or Seminal Fluid
 2-5 mL of fluid expelled during orgasm
 60% seminal vesicle fluid, 30% prostatic, 10% sperm
 normal sperm count 50-120 million/mL
 Other components of semen
 fructose - energy for sperm motility
 fibrinogen causes clotting
 enzymes convert fibrinogen to fibrin
 fibrinolysin liquefies semen within 30 minutes
 prostaglandins stimulate female peristaltic contractions
 spermine is a base stabilizing sperm pH at 7.2 to 7.6
 SPERMATOGENESIS
 SPERMATOGENESIS
 Spermatogonia remain dormant in the
semineferous tubules of the testes since fetal life.
At puberty they become active and begin to
increase in number. The spermatogonia remain in
the adluminal compartment of the seminiferous
tubules between basement membrane and the
sertoli cells.
 The process of spermatogenesis can be divided
into three phases:
 Mitosis: It occurs throughout life. The
spermatogonia increase in number by mitosis.
Two distinct populations of spermatogonia have
been identified. Type A and Type B. Type A
constitute the stem cells. Type are further
classified into dark Type A and light Type A. Dark
Type A are dormant cells and may be long term
reserve cells. The light Type A undergo a series of
mitotic divisions forming Type A1, A2, A3 & A4.
During these divisions the daughter cells remain
connected by cytoplasmic bridges. The Type A4
then transform into Type B spermatogonia. The
type B spermatogonia divide and differentiate
into the primary spermatocytes, the largest germ
cells in the series.
 Spermatogenesis
• Spermatogonia produce 2 kinds of Blood testes
daughter cells barrier

– Type A remain outside

blood-testis barrier and
produce more
daughter cells until death
– Type B differentiate into
primary spermatocytes
• Cells must pass through
BTB to move inward
toward lumen - new tight
junctions form behind
these cells
• meiosis I  2 secondary
spermatocytes
• meiosis II  4
spermatids
 Spermatogenesis
•The primary spermatocytes Blood testes
undergo meiosis to form barrier

spermatozoa.
• meiosis I  2 secondary
spermatocytes each having
haploid number of chromosomes
and are about half the size of the
primary spermatocyte.
•meiosis II  the two secondary
spermatocytes form 4 spermatids
which are about half the size of
the secodary spermatocytes.
 Spermatogenesis
•spermiogenesis: is the
Blood testes
barrier
final stage of spermatogenesis, which
sees the maturation of spermatids
into matre, motile spermatozoa. The
spermatid is more or less circular cell
containing a nucleus, Golgi
apparatus, centriole and
mitochondria.
•The sertoli cells lining the
seminiferous tubules support and
nurture the germ cells and may
be involved in the regulation of
spermatogenesis.
 Spermiogenesis

1. Nucleus condenses (chromosomes condense

and nuclear sap is removed)

2. Flagellum develops

3. Spermatocyte elongates

4. Acrosome formed from golgi body

5. Mitochondria aggregate around base of

forming flagellum

6. Mitochondria fuse to form

supermitochondrion (in humans)

7. Most of cytoplasm is shed and phagocytosed

by sertoli cell (tubulobulbar processes)
 Spermatogenesis
•spermiogenesis: is the
Blood testes
barrier
final stage of spermatogenesis, which
sees the maturation of spermatids
into matre, motile spermatozoa. The
spermatid is more or less circular cell
containing a nucleus, Golgi
apparatus, centriole and
mitochondria.
•The sertoli cells lining the
seminiferous tubules support and
nurture the germ cells and may
be involved in the regulation of
spermatogenesis.
Sperm
 What is involved in the maturation of a sperm cell?
Sperm
Sperm
Sertoli cell function
1. Remove excess cytoplasm from developing
spermatid - tubulobulbar processes
2. Move spermatids toward the lumen of the
seminiferous tubules - ectoplasmic specializations
3. Nurture and mediate maturation of spermatids
4. Segregate groups of developing gametes
5. Secrete fluid to transport sperm in reproductive
tract
6. Secrete hormones and other factors
a. Embryonic - anti-mullarian hormone
b. Adult
(1) inhibin (inhibits FSH production)
(2) estrogen - may act to inhibit GnRH production by
basal hypothalamus
(3) Other factor (not a hormone) - androgen binding
protein (helps transport androgens from interstitial
fluid into seminiferous tubule - promotes
spermatogenesis)
http://education.vetmed.vt.edu/Curriculum/VM8054/Labs/Lab27/EXAMPLES/EXSERTOL.HTM
 Spermatogenesis
The process of Blood testes
barrier

spermiogenesis is
traditionally divided
into four stages: the
Golgi phase, the cap
phase, formation of
tail, and the
maturation stage.
 Spermatogenesis
Golgi phase Blood testes
The spermatids, which up until now have barrier
been mostly radially symmetrical, begin to
develop polarity.
The head forms at one end, and the Golgi
apparatus creates enzymes that will
become the acrosome.
At the other end, it develops a thickened
mid-piece, where the mitochondria gather
and the distal centriole begins to form
an axoneme.
Spermatid DNA also undergoes
packaging, becoming highly condensed.
The DNA is packaged first, with specific
nuclear basic proteins, which are
subsequently replaced with
protamines during spermatid elongation.
The resultant tightly packed chromatin is
transcriptionally inactive.
 Spermatogenesis
Cap phase Blood testes
The Golgi apparatus surrounds the barrier
condensed nucleus, becoming
the Acromosomal cap.
 Spermatogenesis
Formation of Tail Blood testes
One of the centrioles of the cell elongates barrier
to become the tail of the sperm.
During this phase, the developing
spermatozoa orient themselves so that
their tails point towards the center of the
lumen, away from the epithelium.
 Spermatogenesis
Maturation phase
The excess cytoplasm, known as residual
bodies, is phagocytosed by
surrounding Sertoli in the testes
 Spermatogenesis
The whole process of spermatigenesis Blood testes
takes about 64 days. The mature sperms barrier
are released into the lumen of the
seminiferous tubules and are transported
passively into the epididymus. Here they
are stored and become functionally
mature.
Structure of the Gametes: Sperm
 Parts of mature sperm:
 Head Highly Specialized
 Haploid nucleus Cell Type!
 Little cytoplasm
 Acrosome
 Neck/Midpiece
 Mitochondria
 Centriole
 Tail (or propulsion system)
 Some species - ameboid motion
 Most sperm are propelled by flagella
 Formed by microtubles
Figure 7.2(1) The Modification of a Germ Cell to Form a Mammalian Sperm
Internal Sex Organs
Testes
Epididymis
Vas deferens
Seminal vesicles
Prostate gland
Cowper’s glands
History of embryology
Female Reproductive System
Oviduct
Fertilization occurs here
 Gametogenesis in females
 Gametogenesis in females is more complex than the males. The process
begins in the intrauterine life but undergoes a state of maturation
arrest. The process begins again at puberty.
 At puberty the ovary begins to undergo monthly cycles called the
ovarian cycles. During these cycles the a number of gametes restart the
maturation process but only one gamete will mature and will be
released from the ovary.
 The ovarian cycle involves two processes:
 Oogenesis
 Formation of ovarian follicles
 Oogenesis
1) Oogonia are the germ cells that will
eventually develop into the mature
oocytes
2) Primary oocyte : the first step in this
development is the duplication of
homologous chromosomes to get
ready for meiosis
3) Secondary oocyte : the first meiotic
division separates the homologous
chromosomes from each parent
4) Egg: the second meiotic division
separates the 2 chromatids and
creates 4 haploid cells
 In females, it produces 1 egg and 3
polar bodies. This allows the egg to
retain more cytoplasm to support
early stages of development
 Oogenesis
1) Primordial fololicle: a primary oocyte surrounded
by a single layer of flattened epithelial cells.
2) Primary follicle: a primary oocyte surrounded by a
single layer of columnar follicular cells.
3) Secondary follicle : a primary oocyte surrounded
by the cumulus oophoros cells and projecting into
the cavity of a vesicular follicle.
4) Tertiary follicle also called the mature follicle or
graffian follicle: the follicle increased in size with a
large cavity and containing a secondary oocyte
surrounded by the cumulus oophoros cells.
 Oogenesis
• During early fetal life oogonia proliferate by mitotic
division and increase in numbers
• Oogonia enlarge to form primary oocyte
• The primary oocyte becomes surrounded by connective
tissue cells (ovarian stomal cells) which form a single
layer of flattened epithelial cells around the primary
oocyte.
• The primary oocyte surrounded by this layer of cells is
• called the primordial follicle.
• The primary oocyte enters the first meiotic divison but
the process is arrested at the diplotene stage of meiosis I
• The follicular cells secrete a substance called oocyte
maturation inhibitor which keeps meiotic process
arrested.
• At birth almost all the oogonia have differentiated into
primary oocytes. No primary oocytes form after birth.
And the ovaries have a life time stock of primary
oocytes.
# of female germ cells over time
 Oogenesis
 A maximum number of oocytes is reached in the fifth month of
intrauteine life whence the number of germ cells in the ovaries is
around 7 million.
 The germ cells than begin to degenerate, many of the oogonia and
some of the primary oocytes degenerate. The number of germ cells
reduces and at birth there about 2 million primary oocytes.
 The degenerative process continues till puberty and at puberty there
are about 40000 primary oocytes.
 Of these only 400 will reach maturity provided the female does not
take any oral contraceptives.
 The primary oocytes remain in the state of maturation arrest for 15-45
years (menarche to menopause)
 The long duration of maturation arrest may account for the relatively
high frequency of meiotic errors such as non disjunction that occur
with increasing maternal age.
 Oogenesis
• At puberty monthly ovarian cycles begin.
• With each cycle 5-15 follicles begin to mature, only one reaches maturity and
the rest become atretic.
• The primary oocyte enlarges, the surrounding follicular cells become cuboidal
and then columnar. The follicle is now called the primary follicle.
• The primary oocyte soon becomes surrounded by a covering of amorphous
acellular glycoprotein material called the zona pellucida.
 Oogenesis
• The primary oocyte completes its first meiotic division shortly before ovulation
forming the secondary oocyte and the first polar body.
• The secondary oocyte enters the second meiotic division but the process is
again arrested at the metaphase of meiosis II.
• The secondary oocyte will complete its second meiotic division only if it is
fertilized. Otherwise it will degenerate.
• If fertilized, the secondary oocyte and the first polar body divide forming a
mature oocyte and three polar bodies.
 Follicular development
• The follicular cells replicate and the oocyte becomes surrounded by more than
one layer of follicular cells.
• As the primary follicle increases in size the surrounding stromal cells organize
into a capsule the theca folliculi.
• The theca soon differentiates into two layers, an inner vascular and glandular
layer the theca interna and an outer capsular layer the theca externa.
• The thecal cells produce an angiognesis factor that promotes the growth of
blood vessels into the theca interna. Which provides nutrition to the
developing follicle.
• The follicular cells surrounding the secondary follicle continue to proliferate
forming a stratified layer around the oocyte.
• The ovarian follicle soon becomes oval in shape and the oocyte is eccentric in
position in the follicle.
• Soon fluid filled spaces appear around the follicular cells which coalesce to
form a single cavity, the antrum which contains follicular fluid. The follicle is
now called the vesicular or secondary follicle.
• The primary oocyte is pushed to one side of the follicle surrounded by a mound
of follicular cells called the cumulus oophorous, that projects into the cavity of
the enalarged antrum.
 Ovulation
• The mature follicle forms a swelling on the surface of the ovary. Around midcylcle the
ovarian follicle undergoes a growth spurt under the infuence of the FSH and LH. A small
avascular spot soon appears on the surface of this swelling called the stigma.
• On day 14 there is a surge in LH and ovulation follows the LH peak by 12-24 hours.
• The stigma balloons out forming a vesicle which soon ruptures releasing the secondary
oocyte. Expulsion of the oocyte is the result of increased inrtafollicular pressure and
possibly contraction of smooth muscle cells in the theca externa.
• The expelled secondary oocyte is surrounded by zona pellucida and the cumulus
oophorus cells. The cumulus cells now get arranged radially forming the corona radiata.
• Shortly after ovulation the walls of the ovarian follicle become folded and under the
infuence of LH form a gland called the corpus luteum. Which secretes progestrone and
some estrogen. If the oocyte is fertilized the corpus luteum enalrges to form the corpus
luteum of pregnancy. The degeneration of the corpus luteum is prevented by human
chorionic gonadotropin scereted by synctiotrophoblast of the chorion. The corpus
luteum of pregnancy remains active during the first 20 weeks of pregnancy. After which
the placenta starts secreting estrogen and progesterone.
• If fertilization doesnot occur the corpus luteum involutes and degenerates in 10-12 days
and is called the corpus luteum of menstruation. It is subsequently transformed into a
scar tissue called the corpus albicans.
FOLLICULOGENESIS (2)
SELECTION
♥Selection of the dominant follicle occurs day 5-7
♥It depends on
- the intrinsic capacity of the follicle to
synthesize estrogen
-high est/and ratio in the follicular fluid
♥As the follicle mature   estrogen  FSH
“-ve feed back on the pituitary”  the follicle
with the highest No. of FSH receptors will
continue to thrive
♥ The other follicles “that were recruited” will
become atretic
 B

Appearance of LH receptor
on granulosa cells, LH +++

It is considered diploid because there are two shuffled

haploid sets, one goes to ova the other to first polar body
Ready for ovulation

haploid

haploid
 Ovarian Cycle - Follicular
Phase

 Menstruation (day 1) to ovulation(14) (variable)

 Difficult to predict date of ovulation
 Contains menstrual and preovulatory phases
 Thus, in females, the completion of meiosis can be
delayed for over 50 years.
• This is not always good.
• Why not? What could happen?

 Only I egg produced per month (usually)

• What event provides an example of a human the
exception to this?
 In addition, all meiosis is ended in females at
menopause.
In older women, failure of the homologous chromosomes
to separate properly can cause genetic disease
Down syndrome is trisomy 21. It
results in short stature, round face
and mild to severe mental
retardation.

This is the failure of the 2

chromatids to separate during
meiosis 2. It results in one oocyte
receiving 2 instead of 1 chromatid. In
older women, long term association
of chromatids (i.e., over 50 years)
results in the axial proteins failure to
separate.

Down syndrome occurs with a

frequency of 0.2% in women under
30 but at 3% in those over 45 years of
age.
Gilbert Ch. 7 pp. 175-180
Flagella structure
 Must allow sperm to travel long distances, using
plenty of energy
 Axoneme: motor portion
 Microtubules in a 9+2 configuration
 2 central microtubules, 9 doublets
 Made up of the protein tubulin
 Dyenin molecules attach to microtubules and provide
motor activity by hydrolysis of ATP
 Allows filaments to slide and flagellum to bend
Sperm Capacitation
 Upon release, mammalian sperm are able to move, but
do not yet have the capacity to bind an egg
 Must enter the female reproductive tract to complete
the last step of the maturation process (Capacitation)
and acquire the ability to bind the egg
Structure of Gametes: The egg
 Ovum (mature egg) stores all material for
beginning of growth and development
 Unlike sperm, the egg conserves and acquires more
cytoplasm as it matures
 Synthesizes and stores proteins (like yolk) as
reservoirs for the developing embryo
 The components of the egg vary from species to
species
Structure of the gametes: The egg
 PARTS OF THE EGG:
 Cytoplasm - many components
 Haploid nucleus
 Cell membrane
 will fuse with sperm plasma membrane
 Vitelline envelope
 Contains glycoproteins essential for species
specificity & sperm binding
 Zona pellucida (mammals) extra coating made
of Extracellular matrix
Structure of the Gametes: The egg (cont’d)
 Cumulus (mammals): layer of cells that nurture the egg
 Innermost layer is called Corona Radiata
 Cortex
 Beneath the cell membrane
 Gel-like cytoplasm - may help sperm entry into the cell
 Cortical granules
 Inside cortex
 Membrane bound vesicles (like the acrosome in sperm)
 Help prevent polyspermy
 Egg jelly (some species)
 Attract/activate sperm
Sea urchin egg at fertilization
Egg Cytoplasm
 Proteins: energy, amino acids
 mRNA
 To provide early instructions for development
 Ribosomes and tRNA
 To aid in protein synthesis early in development
 Morphogenetic factors
 Molecules that effect differentiation of various cell types
(can be localized to specific areas of the cell)
 Protective Chemicals
 UV filters, DNA repair enzymes, antibodies (birds)
Egg maturation at the time of fertilization in various species
HUMANS
Hamster Eggs Before Fert.
Key Terms
 Diploid: Having the full chromosome number (46 in
humans).

 Haploid: Having half the full chromosome number (23

in humans).
Karyotype
 A karyotype is a
pictorial
representation of a
person’s chromosomes.
 An example is shown
to the right.
 Karyotype
 The X and Y chromosomes
are known as the sex
chromosomes.
 They determine a person’s
gender.
 XX is female, while XY is
male.
 It is the dad who
determines the baby’s
gender as he can produce
sperm carrying the X
chromosome or sperm
carrying the Y
chromosome.
Non-disjunction
 Non-disjunction is the failure of chromosomes (or
tetrads) to separate during anaphase I or II in
meiosis.
 The resulting cells will not have the correct
number of chromosomes.
Non-disjunction
 If it happens in meiosis I, all the resulting cells will be
affected. If it happens in meiosis II, only half will be
affected.
Having extra chromosomes is bad!
 Having too many or
too few chromosomes
is a bad thing.
 Down Syndrome is
caused by having an
extra chromosome 21.
Having extra chromosomes is bad!
 Klinefelter’s Syndrome
occurs when an
individual receives two
X chromosomes and a
Y chromosome.
 The result is an
infertile male with
varying degrees of
feminity.
Missing chromosomes is bad!
 Turner Syndrome occurs
when the individual only
gets one sex chromosome,
an X, from their mother.
 The result is an infertile
female with a broad chest,
poor breast development,
low set ears, short stature
and poor hearing amongst
other things.
Overview of Reproductive System
 Primary sex organs (gonads)
 Produce gametes (testes or ovaries) -
 Gametogenesis - spermatogenesis or oogenesis
 Secondary sex organs
 Male - ducts, glands, penis deliver sperm cells
 Female - uterine tubes, uterus and vagina receive
sperm and nourish developing fetus
 Secondary sex characteristics
 Develop at puberty to attract a mate
 pubic, axillary and facial hair, scent glands, body morphology
and low-pitched voice in males
 Spermatogenesis
• Spermatogonia produce 2 kinds of
daughter cells
– Type A remain outside
blood-testis barrier and
produce more
daughter cells until death
– Type B differentiate into
primary spermatocytes
• Cells must pass through
BTB to move inward
toward lumen - new tight
junctions form behind
these cells
• meiosis I  2 secondary
spermatocytes
• meiosis II  4
spermatids
 Brain-Testicular Axis
 Testicular regulation involves three sets of hormones:
 GnRH - gonadotropin-releasing hormone
 Secreted by hypothalamus
 Stimulates secretion of anterior pituitary secretion hormones (FSH/LH)

 FSH and LH - Follicle stimulating hormone and leuteinizing hormone

 LH aka as Interstitial Cell Stimulating Hormone
 Secreted by anterior pituitary
 Directly stimulate the testes
 FSH - stimulates formation of ABP (androgen binding protein) by nurse cells
 LH - stimulates interstitial cells to secrete testosterone
 Testosterone
 Secreted by cells of Leydig (Interstitial cells of seminiferous tubules)
 Exert negative feedback on hypothalamic and ant. pituitary hormones
 Stimulates spermatogenesis by binding to ABP and development of
secondary sex characteristics
Hormonal Regulation of
Testicular Function
 Feedback inhibition on the
hypothalamus and
pituitary results from:
 Rising levels of
testosterone
 Increased inhibin

Figure 27.10
 Testosterone
 Most from interstitial cells of testes with small amounts from adrenal
glands and sustentacular cells
 Causes enlargement and differentiation of male genitals and reproductive
duct system
 Necessary for sperm cell formation
 Required for descent of testes
 Hair growth on certain parts of the body
 Skin is rougher and coarser
 Quantity of melanin increases
 Increases rate of secretion of sebaceous glands
 Hypertrophy of larynx
 Increases metabolic rate
 Increases red blood cell count
 Increases protein synthesis, rapid bone growth
 Causes closure of epiphyseal plates
Mechanism and Effects of
Testosterone Activity
 Testosterone is synthesized from cholesterol
 It must be transformed to exert its effects on
some target cells
 Prostate – it is converted into dihydrotestosterone
(DHT) before it can bind within the nucleus
 Requires the enzyme 5alpha-reductase
 Neurons – it is converted into estrogen to bring
about stimulatory effects
 Reqires the enzyme aromatase
 Testosterone targets all accessory organs and its
deficiency causes these organs to atrophy
 Accessory Glands
 Seminal vesicles
 Empty into ejaculatory duct
 Produce about 60% of semen
 Secretion contains fibrinogen
 High pH
 Prostate gland
 Produces about 30% of semen
 Thin, milky secretion, high pH
 Contain clotting factors, and fibrinolysin
 Bulbourethral glands
 Contribute about 5% to semen
 Mucous secretion. Just before ejaculation
 Helps neutralize pH of female vagina
 Semen or Seminal Fluid
 2-5 mL of fluid expelled during orgasm
 60% seminal vesicle fluid, 30% prostatic, 10% sperm
 normal sperm count 50-120 million/mL
 Other components of semen
 fructose - energy for sperm motility
 fibrinogen causes clotting
 enzymes convert fibrinogen to fibrin
 fibrinolysin liquefies semen within 30 minutes
 prostaglandins stimulate female peristaltic contractions
 spermine is a base stabilizing sperm pH at 7.2 to 7.6
Semen
 Secretions of all three accessory glands plus
sperm cells referred to as semen.
 Emission: discharge of semen into prostatic
urethra
 Ejaculation: forceful expulsion of semen from
urethra. Caused by peristalsis
 Temporary coagulation as fibrinogen becomes
fibrin then fibrinolysin breaks up the
coagulation. Sperm swim up vagina
 Emission and Ejaculation
 Emission: accumulation of sperm cells and secretions of
the prostate gland and seminal vesicles in the urethra
 Controlled by sympathetic centers in spinal cord
 Peristaltic contractions of reproductive ducts
 Seminal vesicles and prostate release secretions
 Accumulation in prostatic urethra sends sensory
information through pudendal nerve to spinal cord
 Sympathetic and somatic motor output
 Sympathetic: constriction of internal sphincter of urinary bladder so
semen and urine do not mix
 Somatic motor: to skeletal muscles, urogenital diaphragm and base
of penis causing rhythmic contractions that force semen out of
urethra: ejaculation
Neural Control of Erection
Female Reproductive Physiology
Establishing the Ovarian Cycle
 During childhood, ovaries grow and secrete small
amounts of estrogens that inhibit the hypothalamic
release of GnRH
 As puberty nears, GnRH is released; FSH and LH are
released by the pituitary, which act on the ovaries
 These events continue until an adult cyclic pattern is
achieved and menarche occurs
Ovarian Cycle
 Monthly series of events associated with the
maturation of an egg
 Follicular phase – period of follicle growth (days 1–14)
 Luteal phase – period of corpus luteum activity (days
14–28)
 Ovulation occurs midcycle
 Sexual Cycle
 Averages 28 days, ranges from 20 to 45
 Hormone cycle: hierarchy of control
 hypothalamus pituitary  ovaries  uterus
 Follicular phase (2 weeks)
 menstruation occurs during first 3 to 5 days of cycle
 uterus replaces lost endometrium and follicles grow
 Luteal phase (2 weeks)
 corpus luteum stimulates endometrial thickening
 endometrium lost without pregnancy
 Hormonal Interactions During the
Ovarian Cycle
 Day 1 – GnRH stimulates the release of FSH and LH
 FSH and LH stimulate follicle growth and
maturation, and low-level estrogen release
 Rising estrogen levels:
 Inhibit the release of FSH and LH
 Prod the pituitary to synthesize and accumulate these
gonadotropins
 Estrogen levels increase and high estrogen levels have
a positive feedback effect on the pituitary, causing a
sudden surge of LH
Hormonal Interactions During
the Ovarian Cycle
 The LH spike stimulates the primary oocyte to
complete meiosis I, and the secondary oocyte
continues on to metaphase II
 Day 14 – LH triggers ovulation
 LH transforms the ruptured follicle into a corpus
luteum, which produces inhibin, progesterone, and
estrogen
Hormonal Interactions During
the Ovarian Cycle
 These hormones shut off FSH and LH release and
declining LH ends luteal activity
 Days 26-28 – decline of the ovarian hormones
 Ends the blockade of FSH and LH
 The cycle starts anew
Follicular Phase
 The primordial follicle, directed by the oocyte,
becomes a primary follicle
 Primary follicle becomes a secondary follicle
 The theca folliculi and granulosa cells cooperate to
produce estrogens
 The zona pellucida forms around the oocyte
 The antrum is formed
Follicular Phase
 The secondary follicle becomes a vesicular follicle
 The antrum expands and isolates the oocyte and the
corona radiata
 The full size follicle (vesicular follicle) bulges from the
external surface of the ovary
 The primary oocyte completes meiosis I, and the stage is
set for ovulation
 Ovarian Cycle - Follicular
Phase

 Menstruation (day 1) to ovulation(14) (variable)

 Difficult to predict date of ovulation
 Contains menstrual and preovulatory phases
 Ovarian Cycle - Preantral
Phase

 Discharge of menstrual fluid (days 1-5)

 Before follicle develops antrum
 primordial and primary follicles
 Ovarian Cycle - Antral Phase

 Day 6 to 14, one dominant follicle advances to mature (graafian)

follicle; secretes estrogen
Histology of Ovarian Follicles
Ovulation
 Ovulation occurs when the ovary wall ruptures and
expels the secondary oocyte
 Mittelschmerz – a twinge of pain sometimes felt at
ovulation
 1-2% of ovulations release more than one secondary
oocyte, which if fertilized, results in fraternal twins
 Ovarian Cycle - Ovulation

 Mature follicle ruptures, releases oocyte influenced by

LH
Pituitary-Ovarian Axis
Luteal Phase
 After ovulation, the ruptured follicle collapses,
granulosa cells enlarge, and along with internal
thecal cells, form the corpus luteum
 The corpus luteum secretes progesterone and
estrogen
 If pregnancy does not occur, the corpus luteum
degenerates in 10 days, leaving a scar (corpus
albicans)
 If pregnancy does occur, the corpus luteum
produces hormones until the placenta takes over
that role (at about 3 months)
 Ovarian Cycle - Luteal Phase

 Corpus luteum - forms from ruptured follicle, under influence of

LH; secretes progesterone
Menstrual Cycle - Proliferative Phase

 Day 6-14 rebuild endometrial tissue

 mitosis occurs in stratum basalis
 result of estrogen from developing follicles
Uterine (Menstrual) Cycle
 Series of cyclic changes that the uterine
endometrium goes through each month in
response to ovarian hormones in the blood
 Days 1-5: Menstrual phase – uterus sheds all but
the deepest part of the endometrium
 Days 6-14: Proliferative (preovulatory) phase –
endometrium rebuilds itself
 Days 15-28: Secretory (postovulatory) phase –
endometrium prepares for implantation of the
embryo
Menses
 If fertilization does not occur, progesterone levels
fall, depriving the endometrium of hormonal
support
 Spiral arteries kink and go into spasms and
endometrial cells begin to die
 The functional layer begins to digest itself
 Spiral arteries constrict one final time then
suddenly relax and open wide
 The rush of blood fragments weakened capillary
beds and the functional layer sloughs
Gonadotropins, Hormones, and the Ovarian and
Uterine Cycles

Figure 27.22a, b
Gonadotropins, Hormones, and the Ovarian and
Uterine Cycles

Figure 27.22c, d
Extrauterine Effects of Estrogens and
Progesterone

 Estrogen levels rise during puberty

 Promote oogenesis and follicle growth in the ovary
 Exert anabolic effects on the female reproductive tract
 Uterine tubes, uterus, and vagina grow larger and
become functional
 Uterine tubes and uterus exhibit enhanced motility
 Vaginal mucosa thickens and external genitalia
mature
Estrogen-Induced Secondary
Sex Characteristics
 Growth of the breasts
 Increased deposition of subcutaneous fat, especially in
the hips and breasts
 Widening and lightening of the pelvis
 Growth of axillary and pubic hair
From Egg to Embryo
 Pregnancy – events that occur from fertilization until the
infant is born
 Conceptus – the developing offspring
 Gestation period – from the last menstrual period until
birth
 Preembryo – conceptus from fertilization until it is two
weeks old
 Embryo – conceptus during the third through the eighth
week
 Fetus – conceptus from the ninth week through birth
Accomplishing Fertilization
 The oocyte is viable for 12 to 24 hours
 Sperm is viable 24 to 72 hours
 For fertilization to occur, coitus must occur no more
than:
 Three days before ovulation
 24 hours after ovulation
 Fertilization – when a sperm fuses with an egg to form
a zygote
Sperm Transport and
Capacitation
 Fates of ejaculated sperm
 Leak out of the vagina immediately after deposition
 Destroyed by the acidic vaginal environment
 Fail to make it through the cervix
 Dispersed in the uterine cavity or destroyed by
phagocytic leukocytes
 Reach the uterine tubes
 Sperm must undergo capacitation before they can
penetrate the oocyte
Acrosomal Reaction and Sperm
Penetration
 An ovulated oocyte is encapsulated by:
 The corona radiata and zona pellucida
 Extracellular matrix
 Sperm binds to the zona pellucida and undergoes the
acrosomal reaction
 Enzymes are released near the oocyte
 Hundreds of acrosomes release their enzymes to digest
the zona pellucida
Acrosomal Reaction and Sperm
Penetration
 Once a sperm makes contact with the oocyte’s
membrane:
 Beta protein finds and binds to receptors on the oocyte
membrane
 Alpha protein causes it to insert into the membrane
Acrosomal Reaction and
Sperm Penetration

Figure 28.2a
Blocks to Polyspermy
 Only one sperm is allowed to penetrate the oocyte
 Two mechanisms ensure monospermy
 Fast block to polyspermy – membrane depolarization
prevents sperm from fusing with the oocyte membrane
 Slow block to polyspermy – zonal inhibiting proteins
(ZIPs):
 Destroy sperm receptors
 Cause sperm already bound to receptors to detach
 Implantation
 Viability of the corpus luteum is maintained by human
chorionic gonadotropin (hCG) secreted by the
trophoblasts
 hCG prompts the corpus luteum to continue to secrete
progesterone and estrogen
 Chorion – developed from trophoblasts after
implantation, continues this hormonal stimulus
 Between the second and third month, the placenta:
 Assumes the role of progesterone and estrogen production
 Is providing nutrients and removing wastes
Hormonal Changes During Pregnancy

Figure 28.6
Parturition: Initiation of Labor

Figure 28.16
Female Reproductive System
Lastly the
sperm and
egg meet
here for
fertilization

Sperm must
pass through
the uterus 2nd

Sperm Enters
the vagina 1st
Oviduct
Fertilization occurs here
Ovary: Details of Histology &
Physiology

Figure 26-12d: ANATOMY SUMMARY: Female Reproduction

 Diploid cell In embryo

Differentiation and
onset of MEIOSIS I

PRIMARY OOCYTE,

arrested at diplotene stage of the prophase of Present at birth

MEIOSIS I

Completion of MEIOSIS I
and onset of MEIOSIS II

SECONDARY OOCYTE,
First
arrested at metaphase
polar body
of MEIOSIS II;
released from ovary

Entry of sperm triggers

completion of MEIOSIS II

OVUM
Second
(haploid) polar body

Figure 27.4B
 Development of an ovarian follicle

Degenerating Start: PRIMARY OOCYTE

corpus luteum
within follicle
CORPUS LUTEUM

Growing
follicles

Mature follicle

SECONDARY Ovary
OOCYTE
OVULATION Ruptured follicle Figure 27.4C