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Dr. dr. Eko Poerwanto., M.Kes.

, AIFM

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Reproduction
Reproductive System
Not needed for the survival of the individual (!!!)
Species survival

Sexual reproduction
Genes from two individual
Combine at random
Creates new combinations
Increases chances of species survival

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Sexual Reproduction
Each individual produces gametes
Formed in gonads by meiosis
Male: testes produce:
Sperm
Testosterone

Female: ovaries produce:


Ova
Estrogens, Progesterone

Gametes unite in process of fertilization


Restores diploid number
Forms zygote

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Sexual Determination
Each zygote inherits
23 chromosomes from mother
23 chromosomes from father.
23 pairs of homologous chromosomes.
alleles

Kinds of chromosomes
1-22 pairs of chromosomes: autosomal
23rd pair are sex chromosomes.
Male: XY
Female: XX

Chromosomal gender of zygote determined


by fertilizing sperm.(X / Y)
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Formation of Testes
First 40 days after conception the gonads of males
and females are similar in appearance.
During this time:
Spermatogonia and oogonia migrate from yolk sac to
developing embryonic gonads
Gonads could become either.
TDF (testis-determining factor):
hypothetical
promotes the conversion to testes:
gene located on short arm of Y, called SRY (sex determining region
of Y chromosome)
Found in all mammals
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Formation of Testes
Structures in the testes:
Seminiferous tubules: 43 to 50 days post conception
Germinal cells: sperm.
Nongerminal cells: Sertoli cells (sustentacular cells).

Leydig cells (interstitial cells):


Appear about day 65.
Endocrine function: secrete androgens
Main: Testosterone

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Formation of Testes
Leydig cells secrete testosterone.
Begins 8th week and peaks at 12-14th week.
Masculinizes embryonic structures.
Testosterone then declines to very low levels
until puberty.
Decline occurs by end of second trimester
Testes descend into scrotum shortly before
birth.
Temp about 3 degrees below internal temp
35 oC

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Formation of Ovaries
Absence of Y chromosome and TDF, female develop
ovaries.
Ovarian follicles do not appear until 2nd trimester.

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Development of
Accessory Sex Organs & Genitalia
Presence or absence of
testes determines the
accessory sex organs and
external genitalia.
Male accessory organs
derived from wolffian
ducts.(mesonephric)
Sertoli cells secrete
MIF(mullerian
inhibition factor).
Female accessory organs
derived from mullerian
ducts.
(paramesonephric)
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Development of
Accessory Sex Organs & Genitalia
Both duct systems in both sexes between days 25
and 50
Regression of mullarian ducts begins about day 60

Testosterone
responsible for development of male accessory sex
organs
External genitalia identical first 6 weeks, then
testosterone stimulates development of penis
Not the active agent in all cells
converted to dihydrotestosterone (DHT) in some target cells
Needed for penis, spongy urethra, scrotum, prostrate

Testosterone directly needed for wolfian derivatives:


Epididymis, ductus deferens, ejaculatory duct, Seminalis Vesicula

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Development of Accessory Sex Organs and
Genitalia

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Endocrine Regulation of Reproduction
First trimester
Embryonic testes are active endocrine glands
Secrete large amounts of testosterone
Embryonic ovaries not mature until third trimester

Time of birth:
Gonads in both sexes relatively inactive

Before puberty:
Low levels of sex steroids in both
Due to lack of stimulation

Puberty:
Increased stimulation from gonadotropic hormones
Induce increase in sex steroids
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Endocrine Regulation of Reproduction
Hypothalamus releases LHRH (GnRH) into
hypothalamo-hypophyseal portal vessels.

Anterior pituitary secretes:


LH: luteinizing hormone.
In male: interstitial-cell stimulating hormone (ICSH)
FSH: follicle-stimulating hormone.

Secreted in pulsatile mode to prevent


desensitization and down regulation of receptors.

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Endocrine Interactions
Primary effects of LH and FSH on
gonads:
Stimulation of spermatogenesis and
oogenesis.
Stimulation of gonadal hormone
secretion.
Maintenance of gonadal structure.

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Endocrine Regulation
Negative Feedback:
Inhibit GnRH from
hypothalamus.
Inhibit anterior pituitary
response to GnRH.
Inhibin secretion inhibit
anterior pituitary release
of FSH.
By sertoli cells ()

Female: estrogen and


progesterone.
Male: testosterone.

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Onset of Puberty
FSH and LH high in newborn, falls to low levels in
few weeks.

Puberty: driven by increased secretion of FSH


and LH

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Onset of Puberty
FSH & LH
Brain maturation increases GnRH secretion.
Decreased sensitivity of GnRH to negative feedback.
LH:
Increased secretion triggers puberty
Late puberty, pulsatile secretion of LH and FSH
increase during sleep.
Stimulate a rise in sex steroid secretion.

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Onset of Puberty
Stimulate rise in
testosterone and
estradiol-17.
Produce secondary
sexual characteristics.
Age of onset related to
the amount of body fat
and physical activity in
the female
Leptin secretion from
adipocytes may be
required for puberty.

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Male Reproduction System
Testes:
Seminiferous tubules:
Where spermatogenesis
occurs.
Contain receptor proteins
for FSH in Sertoli cells.

Leydig cells:
Secrete testosterone.
Contain receptor proteins
for LH.

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Control of LH and FSH Secretion
Negative feedback:
Testosterone inhibits
LH and GnRH
production.
Inhibin inhibits FSH
secretion.
Aromatization reaction
producing estradiol in
the brain is required for
the negative feedback
effects of testosterone
on LH.
Brain is a target organ for
testosterone
Converted to derivatives

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Testosterone Secretion
Responsible for initiation
and maintenance of body
changes in puberty.

Stimulate growth of
muscles, larynx, and bone
growth until sealing of the
epiphyseal discs.

Promote hemoglobin
synthesis.

Acts in paracrine mode


and is responsible for
spermatogenesis.

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Testosterone Secretion
Negative feedback of testosterone and inhibin
Keep relatively constant levels of gonadotropins
Results in relatively constant levels
Different in female
At menopause: no more sex steroids (estrogen /progesteron)
In males, gradual decrease

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Endocrine function: testes
Testosterone: main androgen

Sertoli & Leydig cells secrete small amounts of


estradiol.
Have receptors for estradiol (as do other male structures)
May be needed for spermatogenesis

Estradiol may be responsible for:


Negative feedback in brain.
Sealing of epiphyseal plates.
Regulatory function in fertility.

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Spermatogenesis
Spermatogonia:
Replicate initially by mitosis.
Produce two cells

One becomes a primary spermatocytes undergoes


meiosis:
2 nuclear divisions.
2nd meiotic division produce 4 spermatids.

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Spermiogenesis
Maturation of
spermatozoa.
Spermatozoa is
pinched off and
ingested by the
Sertoli cell
cytoplasm.

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Sertoli Cells
Blood-testes barrier:
Prevents autoimmune destruction of sperm.
Produce FAS ligand which binds to the FAS receptor
on surface to T lymphocytes, triggering apoptosis.
Secretes inhibin.
Phagocytize residual bodies:
Transmit information molecules from germ cells to
Sertoli cells.
Secrete ABP (androgen-binding protein):
Binds to testosterone and concentrates testosterone in
the tubules.

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Hormonal Control of
Spermatogenesis
Testosterone required for
completion of meiosis and
spermatid maturation.

Testes secrete paracrine


regulators:
IGF-1.
Inhibin.

FSH necessary in the later


stages of spermatid
maturation.

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Male Accessory Organs
Epididymis:
Maturational changes.
Resistance to pH changes and temperature.
Storage.

Prostate secretes:
Alkaline fluid.
Citric acid.
Ca++.
Coagulation proteins.

Seminal vesicles secrete:


Fructose.
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Erection, Emission, and Ejaculation
Erection:
Increased vasodilation of arterioles.
Blood flow into the erectile tissues of the penis.
Parasympathetic

Emission:
Movement of semen into the urethra.
Sympathetic

Ejaculation:
Forcible expulsion of semen from the urethra out of the
penis.
Sympathetic

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Ejaculation:

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