Ch. 20 Reproduction (Day 1) Flashcards
What are the 2 types of cells in the human life cycle?
- Germ cells
- -ova, sperm - Somatic cells
- -everything else in the body
Gametogenesis: Males vs. Females
Males: large numbers of gametes produced continuously from stem cells, beginning at puberty and extending until senescence (age-dependent decrease in testosterone production)
Females: release only ONE gamete at a time from limited pool of preformed gametes in a process that is repeated at regular monthly intervals
Where does gametogenesis begin?
In utero - mitotic divisions to increase germ cell numbers; PAUSES at birth and RESUMES at puberty
Timing varies between males and females
Spermatogenesis
- Spermatogonium DNA replicates but no division to form primary spermatocyte (46 chromosomes to 92) at PUBERTY
–MEOISIS 1 OCCURS–
- Primary spermatocyte splits into 2 secondary spermatocytes (46 chromosomes each)
–MEIOSIS 2 OCCURS–
- The 2 secondary spermatocytes split into 4 spermatids (23 chromosomes each), which mature into sperm via spermiogensis
- Sperm have 23 chromosomes each, released from tests during “spermiation”
Oogensis
- Oogonium (46 chromosomes) DNA replicates but no division into Primary Oocyte (92 chromosomes)
–MEIOSIS 1 OCCURS (puberty)–
- primary oocyte splits into 1 secondary oocyte (46 chromosomes) and 1 polar body (dies)
- secondary oocyte begins Meiosis 2 and is released during ovulation
- secondary oocyte splits into 1 Ootid (23 chromosomes) and 1 polar body (23 chromosomes, dies)
5a. Meiosis 2 is completed ONLY IF FERTILIZATION OCCURS
5b. If fertilization doesn’t occur, Ootid dies (?)
Oocyte production
- Primary oocyte
- a) toward end of gestation, female’s oogonia begin meiosis to produce PRIMARY OOCYTES
- b) ovaries of newborn girl have 2 million primary oocytes
- c) by puberty, this number is cut to ~400,000
- d) only about 400 of these will be ovulated in her lifetime - Primary oocytes contained w/in primary follicles - have one layer of cells
- a) in response to FSH, some of primary follicles grow to produce many layers of granulosa cells (granulose cells support developing oocyte in middle of that follicle)
- b) some develop fluid-filled vesicles called secondary follicles - Continued growth results in fused vesicles to form single atrium; this is a mature Graafian follicle
- As Graafian follicle grows, primary oocyte finishes meiosis 1 to become secondary oocyte (plus a polar body, which soon degenerates)
- Secondary oocyte begins meiosis 2, but stops at metaphase 2
- Meiosis 2 will complete, ONLY if there is fertilization of ovum
Is it the sperm or egg that determines genetic sex of zygote?
Sperm
Sex determination in embryo
If zygote contains Y chromosome: male (even if multiple X’s)
If zygote gets only Y but no X –> lethal b/c X chromosome is essential for survival
X-inacitvation in females: early in development, after ovaries develop, one X in each body inactivates (becomes Barr body) - inactivation is random - some may be sperm-derived, others ovum-derived
Are polar bodies and Barr bodies the same?
No, they’re 2 different bodies
Why does X-inactivation occur in females (Barr body)?
So that only one X is viable in gamete (for reproduction later on in life)
random inactivation of one of X chromosomes
Chromosomal sex and development of embryonic gonads
Genetic sex is determined by which sex chromosome is carried by the sperm (X or Y)
Key gene carried on Y chromosome: “Testis Determining Factor” (TDF), aka “Sex Determining Factor” (SRY)
If sperm contributes Y: SRY expression stimulates testis differentiation
If sperm contributes X: lack of SRY allows ovary differentiation
The presence/absence of what gene on the sperm determines genetic sex?
SRY (aka TDF) gene
Presence of SRY = male
Absence of SRY = female
Sexual differentiation occurs early in development - internal organs
Regardless of genetic sex, embryo has potential to become phenotypically male or female - female pattern occurs unless humoral signals are released from fetal testis
Depends on presence of SRY gene on Y chromosome
If female: no SRY gene, biopotential gonads –> ovaries
If male: SRY expression elicits gonads –> testes
Testes produce masculinization factors (testosterone, anti-Müllerian hormone [AMH])
Wolffian Duct
Male
Degenerates if SRY isn’t present; develops if SRY is present
Müllerian Duct
Female
Degenerates if SRY is present; develops [ovaries, female reproductive organs] if SRY is NOT present
T/F: Testes secretion of testosterone is what determines if embryo is male or female.
FALSE
Testes secretion of testosterone is NOT what determines genetic sex - it’s the presence/absence of SRY gene expression that determines genetic sex
If SRY gene is present, testes develop and then testosterone is secreted
Leydig Cells
Males
Secrete testosterone
Controls development of Wolffian duct into accessory structures, development of external male genitalia (via DHT)
Sertoli Cells
Males
Secrete Anti-Müllerian hormone
Causes regression of Müllerian duct
T/F: Testosterone is NOT produced until testes differentiate
True
Sexual differentiation
Production of dihydrotestosterone (DHT) required for development of male external genitalia
Masculinization
Due to testosterone
Converted to DHT (dihydrotestosterone)
Changes occur in brain development
From birth to puberty - period of reproductive senescence
Testes stop producing testosterone by 3rd trimester; ovaries don’t produce embryonic sex hormones
Sex hormone secretion does NOT resume in either sex until gonads are stimulated at puberty
Onset of puberty: anterior pituitary begins releasing gonadotropic hormones
Onset of puberty
Secretion of FSH and LH is elevated at birth and stays high for the first 6 months of postnatal life; declines to almost nothing until puberty
Puberty begins w/ release of LH (pulsatile)
- a) results in increases in testosterone or estradiol-17beta secretion
- b) these hormones produce secondary sex characteristics
- -> females: growth spurt, breast development, menarche
- -> males: growth spurt, muscle, penis and testis growth
- -> both females and males: body hair - all stimulated by adrenal androgens
What is menarche?
First menstruation
Puberty
Maturation of hypothalamic-pituitary axis - seems to be associated w/ childhood nutrition - age of menarche has decreased in Western societies as energy intake has increased
Pulsatile secretion of GnRH increases –> increase in secretion of LH and FSH
As energy intake increases –> increased storage of TG in adipose –> increased leptin secretion
Leptin goes from adipose tissue to both hypothalamus and pituitary, which promotes release of GnRH and eventually secretion of LH and FSH which act on reproductive organs
Growth as a function of sex and age
Age of onset of puberty:
- depends on activity levels and amount of body fat
- leptin secreted by adipose cells required for onset
- exercise may inhibit GnRH secretion
- more active, slimmer girls begin puberty later
- melatonin from pineal gland may play role, but this is not proven in humans
Interaction between hypothalamus, anterior pituitary, and gonads
Follicle-Stimulating hormone (FHS) and luteinizing hormone (LH) produced in anterior pituitary glands (males and females) - 3 effects:
- 1) stimulation of spermatogenesis or oogenesis
- 2) stimulation of gonadal hormone secretion
- 3) maintenance of structures of gonads
Release of FSH and LH controlled by release of gonadotropin-releaseing hormone (GnRH) from hypothalamus
Regulated by negative-feedback loop where rising levels of gonadal hormone
- 1) inhibit GnRH release
- 2) inhibit pituitary response to GnRH
Hormonal Control of Reproduction
GnRH release is pulsatile in both males and females (more so in females; pulses every 1-3 hours)
LH, FSH act via feedback inhibition on GnRh release
Release of LH, FSH stimulated by low levels of gonadal steroids; when steroids increase, usually get feedback inhibition of LH, FSH
BUT if estrogen greatly increases can get stimulation of gonadotropin (LH) release
Male Reproduction - Gross Anatomy
Accessory glands (seminal vesicles, prostate, bilbo-urethral glands) - secrete fluids which lubricate tubular system and nutrients (e.g. fructose) to support energy usage by sperm. Fluid from seminal vesicles constitutes to about 70% of sperm volume
Placement of testis outside abdominal cavity maintains 2-3ºC
Duct of Epididymis
Site of maturation and storage of sperm; FSH receptors (on sertoli cells)
Seminiferous Tubule
Site of sperm production
During arousal and ejaculation, contractions of circular smooth muscle around epididymal duct advance sperm into ____ ____ and ultimately the ____.
Vas Deferences; urethra
Spermatogenesis in seminiferous tubules
Leydig cells - produce and secrete testosterone in response to LH; active in fetus, virtually disappear after first 6 months of postnatal life; reappear w/ onset of puberty
Sertoli cells - regulation of sperm development - secrete proteins necessary for sperm development (e.g. androgen-binding protein) in response to FSH and testosterone
T/F: Sperm have receptors for testosterone.
FALSE
Sertoli cells are the ones that have testosterone receptors
Hormonal control of spermatogenesis
negative feedback effects of testosterone and inhibin maintain relatively constant secretion of gonadotropin in males
Androgen secretion decreases slowly in females to hypogonadal state by age 70
Other factors affecting testosterone secretion: physical inactivity, obesity, drugs
Fimbriae
female
partially wrap around ovaries, “catch” oocytes after ovulation
Fallopian tube
female
ciliary action moves egg from ovary toward uterus; dysfunction can result in infertility or ectopic pregnancy
Uterus
female
normal site of implantation and development of fertilized egg
Cervix
female
cervical canal lined w/ mucus-secreting cells - mucus forms protective barrier between vagina and uterus
Endometrium
female
innermost tissue layer in uterus; epithelial thickness and character vary during menstrual cycle - cells progress through monthly cycles of proliferative, secretory, and menses phases coinciding w/ ovarian cycle
Myometrium
female
middle muscle layer in uterus; contracts to expel baby at birth
Perimetrium
female
outer CT layer in uterus
Follicular development - ovarian cycle
Preovulatory phase
-follicle developing under influence of steadily rising levels of estrogen
When estrogen levels peak, induces surge of LH which induces ovulation
Postovulatory (luteal phase)
-corpus luteum (remnants of ruptured follicle egg was released from in ovulation) secretes hormones which help prepare for pregnancy
If no pregnancy, corpus luteum degenerates and cycle resumes
What happens when fertilization of the egg does NOT occur?
Corpus luteum survives for about 12 days
If no pregnancy, C.L. undergoes apoptosis, becomes inactive (corpus albicans)
As luteal cells die, secretion of estrogen and progesterone decreases
As progesterone levels decrease blood supply to endometrium is compromised, surface epithelium begins to die
2 days after C.L. ceases fxn (14 days after ovulation), endometrium begins to slough its surface layer & menstruation begins—lasts from 3-7 days
As steroids decrease negative feedback on hypox, pituitary, so GnRH –> FSH, LH increase
Increasing FSH, LH induce start of the next ovulatory cycle (during menstrual cycle
Follicular phase - early
Follicular development begins under influence of FSH
As follicle matures, FSH and LH stimulate granulose cells and thecal cells, respectively, to produce androgens
Granulose cells also produce AMH which limits number of follicles development at a time by decreasing their sensitivity to FSH
Thecal cells synthesize androgens –> diffuse to granulose cells –> covert androgens –> estrogens
Follicular Phase - mid-late
At the same time, estrogen stimulates its own production by granulose cells
Menstruation ends during early follicular phase
In response to rising estrogen, new endometrium begins to grow - increased cell number, enhanced blood supply
As follicles enlarge, granulosa cells secrete fluid that collects in cavity in follicle (atrum). Fluid contains factors needed for ovulation
Ovulatory Phase
ovarian estrogen rises to a peak, its effect now changes to strong STIMULATORY effect on GnRH –> FSH, LH - get huge surge in LH
increased estrogen levels also stimulates growth of endometrium to max thickness
Mature follicle secretes enzymes which break down ECM holding follicular cells together; breakdown products induce inflammatory response - neutrophils secrete prostaglandins –> contraction of smooth muscle in outer thecal layer, rupturing follicle wall –> egg is extruded
Post-ovulatory (LUTEAL) phase
LH surge also causes remaining thecal and granulosa cells to migrate into antrum –> transform into luteal cells, remaining structure is corpus luteum (C.L.)
C.L. secretes estrogen, highly increases progesterone and inhibin levels - negative feedback on hypothalamus and pituitary - gonadotropin secretion shut down
Progesterone promotes further development of endometrium to support pregnancy, also promotes thickening of cervical mucus to protect uterus
Progesterone elicits rise in basal body temp (~0.3ºC) which lasts until onset of menstruation
