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1._General_Reproduction.pdf King CAESOR UNIVERSITY
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- 2. Sexual Reproduction • Genesfrom two individuals are combined in random ways to produce a new individual. – Allows for genetic variation and adaptability to a changing environment
- 3. Sexual Reproduction • Germcells become gametes (sperm and ova) in the gonads via meiosis. • Ova and sperm are fused in fertilization. • The new individual progresses from zygote → embryo → fetus.
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- 5. Chromosomes • Each zygotegets 23 chromosomes from mom and 23 from dad. – Produces 23 pairs of homologous chromosomes – 22 pairs are autosomal chromosomes = have the same (but not identical) genes on them. – The last pair are the sex chromosomes.
- 6. Sex Chromosomes • Femaleshave two X chromosomes. – Mom always passes on an X chromosome. • Males have an X and a Y chromosome. – Dad can pass on either an X or a Y chromosome. – The sex of a child is determined by the contributing sperm.
- 7. Sex Chromosomes • Xand Y look different and have different genes. – X has 1,090 genes while Y has only 80 genes. – The Y chromosome has many testis-specific genes.
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- 9. Sex Chromosomes • Infemales, one of the two X chromosomes is inactive. – This produces a visible Barr Body. – This is an easy way to visually determine the sex of a cell.
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- 11. Formation of Gonads •After fertilization, the gonads and associated structures are identical in males and females. – Embryonic gonads can become either testes or ovaries. – The signal that determines which is called testis-determining factor (TDF). – This is coded for by a gene on the Y chromosome.
- 12. Formation of Testes •Soon after the production of TDF in XY embryos, the seminiferous tubules form. – Germinal cells and Sertoli cells differentiate 45−50 days after fertilization. – The Leydig cells (those that make testosterone) appear around day 65.
- 13. Formation of Testes •The Leydig cells begin making large amounts of testosterone ~8 weeks after fertilization. – This stimulates the development of the rest of the male reproductive organs. • As the testes develop, they descend into the scrotum.
- 14. Formation of Ovaries •Without TDF, XX embryos do not develop testes. • Follicular cells do not appear until the second trimester.
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- 16. Formation of AccessorySex Organs • Between days 25 and 50, both male and female embryos have two systems of ducts: – Wolffian ducts: can become male tract – Mullerian ducts: can become female tract
- 17. Formation of AccessorySex Organs • In the growing testes, the Sertoli cells secrete Mullerian-inhibiting factor. – This makes the Mullerian duct regress. – Testosterone from the Leydig cells stimulates the development of the Wolffian duct (epididymis, ductus deferens, seminal vesicle). – Without this inhibition and stimulation, the Mullerian ducts develop into fallopian tubes and a uterus.
- 18. Formation of ExternalGenitalia • Identical in males and females for first 6 weeks of life – Both sexes have a urogenital sinus, labioscrotal swelling, genital tubercle, and urethral fold. – Testosterone masculinizes these into the scrotum, prostate gland, and penis. – Without testosterone, these become the labia and clitoris.
- 19. Development of ExternalGenitalia
- 20. Regulation of SexualDevelopment
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- 22. Disorders of SexualDevelopment • Hermaphroditism: Both ovarian and testicular tissue exist in the body. – Some people have an ovary on one side and a testis on the other, while others have fused ovotestes. – Due to a problem in zygotic mitosis, not every cell receives the full Y chromosome.
- 23. Disorders of SexualDevelopment • Pseudohermaphroditism: The individual has ovaries or testes, but accessory structures are not complete or are inappropriate for the genetic sex. – Female pseudohermaphroditism: may be due to excessive secretion of adrenal androgens in a female = congenital adrenal hyperplasia. • Both Mullerian and Wolffian duct derivatives and male external genitalia
- 24. Disorders of SexualDevelopment – Male pseudohermaphroditism: may be due to testicular feminization syndrome whereby testes make testosterone but testosterone receptors don’t work. • Female external genitalia form, but there is no uterus or fallopian tubes because the Mullerian duct still degenerated. • There is no male tract either because the Wolffian duct was not stimulated.
- 25. Disorders of SexualDevelopment – Male pseudohermaphroditism: may also occur because of inability to make the enzyme 5α-reductase, which converts testosterone into DHT in target cells. • This is required for masculinization of external genitalia.
- 26. Disorders of SexualDevelopment
- 27. II. Endocrine Regulationof Reproduction
- 28. Sex Hormone Secretion •The testes stop making testosterone by the third trimester, and the ovaries don’t make embryonic sex hormone. • Sex hormone secretion does not occur again in either sex until the gonads are stimulated at puberty. • At this time, the anterior pituitary begins releasing gonadotropic hormones.
- 29. Gonadotropic Hormones • Follicle-stimulatinghormone (FSH) and luteinizing hormone (LH) are produced in both males and females with three effects: 1. Stimulation of spermatogenesis or oogenesis 2. Stimulation of gonadal hormone secretion 3. Maintenance of the structures of the gonads
- 30. Regulation of FSHand LH • Release of FSH and LH is controlled by the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. • Regulated by a negative-feedback loop where rising levels of gonadal hormone: – Inhibit GnRH release – Inhibit pituitary response to GnRH
- 31. Regulation of FSHand LH • Aside from the usual gonadal hormones (testosterone, estrogen, and progesterone), the gonads also secrete inhibin. – Secreted by Sertoli cells in testes – Secreted by granulosa cells of ovarian follicles – Specifically inhibits release of FSH (no effect on LH)
- 32. Regulation of Hormones •Similar in males and females, but male secretion is constant while female secretion is cyclical. • At one point in the female cycle, estrogen has a positive effect on LH release.
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- 34. Puberty • Secretion ofFSH and LH is elevated at birth and stays high for the first 6 months of postnatal life. – This declines to almost nothing until puberty. • Puberty begins with a release of LH. – This results in increases in testosterone or estrogen secretion. – These hormones produce secondary sex characteristics.
- 35. Secondary Sex Characteristics •In girls: growth spurt, breast development, menarche (first menstrual flow) • In boys: occurs later; body, muscle, penis, and testis growth • In both sexes: body hair is stimulated by androgens from adrenal gland at puberty
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- 37. Female Sexual Development atPuberty
- 38. Male Sexual Development atPuberty
- 39. Onset of Puberty •Depends on activity levels and amount of body fat – Leptin secreted by adipose cells is required for the onset of puberty. – Exercise may inhibit GnRH secretion. – More active, slimmer girls begin puberty later. – Melatonin from the pineal gland may play a role, but this is not proven in humans.
- 40. Human Sexual Response •Four phases: 1. Excitation: characterized by increased muscle tone, vasocongestion of sexual organs; also called arousal 2. Plateau: continued vasocongestion 3. Orgasm: contraction of the uterus/vagina and male ejaculatory organs 4. Resolution: body returns to pre-excitation condition • Men experience a refractory period.
- 41. III. Male ReproductiveSystem
- 42. Testes • Have twocompartments: – Seminiferous tubules: where spermatogenesis occurs • FSH receptors are found here, on Sertoli cells. • FSH influences spermatogenesis. – Interstitial tissue: where Leydig cells make testosterone; also filled with blood and lymphatic capillaries • LH receptors found here on Leydig cells • Testosterone secreted in response to LH
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- 44. Gonadotropin Secretion • LHsecretion is controlled by rising testosterone secretion through negative feedback. • FSH secretion is controlled by testosterone and inhibin secretion. – Inhibin is released from the Sertoli cells of the seminiferous tubules.
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- 46. Testosterone in theBrain • Testosterone is converted to its derivatives in brain cells. – Converted by 5α-reductase to DHT or to estradiol by aromatase enzyme – Estradiol is used to inhibit LH secretion.
- 47. Testosterone in theBrain
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- 49. Spermatogenesis • Diploid spermatogoniafirst go through mitosis. • One of the daughter cells (the primary spermatocyte) continues through meiosis. • After meiosis I → 2 secondary spermatocytes. • After meiosis II → 4 spermatids.
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- 52. Spermiogenesis • Maturation ofspermatids into functioning spermatozoa – Mature spermatozoa have a flagellum, head, midpiece, and acrosome cap.
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- 54. Spermiogenesis and SertoliCells • Sperm development requires Sertoli cells. – Sertoli cells create a blood-testis barrier controlling what can enter the seminiferous tubules and preventing the immune system from developing antibodies against the sperm. – They also secrete FAS ligand, which binds to an FAS receptor on T cells, stimulating apoptosis. • This creates an immunologically privileged site.
- 55. Spermiogenesis and SertoliCells • Sertoli cells envelop the developing sperm. – They phagocytize some of the spermatid cytoplasm in spermiogenesis. – They secrete androgen-binding protein (ABP) into the seminiferous tubule lumen. This binds to testosterone and concentrates it in the tubule. • ABP production is stimulated by FSH. • Testosterone stimulates spermatogenesis and spermiogenesis.
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- 58. Hormonal Control of Spermatogenesis •Testosterone is required to stimulate meiosis and early spermatid maturation. – Testosterone is secreted by the Leydig cells after stimulation by LH. – FSH enhances spermatogenesis through the action of the Sertoli cells that are stimulated to make ABP, which concentrates the testosterone levels. • FSH ensures optimal fertility
- 59. Male Accessory SexOrgans • Spermatids move from the seminiferous tubules → rete testis → efferent ductules → epididymis. • The epididymis is the site of sperm maturation and storage. • In ejaculation, spermatozoa move from the epididymis → ductus deferens → ejaculatory duct → urethra.
- 60. Male Accessory SexOrgans • The seminal vesicle and prostate gland add fluid to the sperm to form semen. – Seminal fluid: contains fructose (energy for sperm) – Prostate fluid: contains citric acid, calcium, and coagulation proteins
- 61. Male Accessory SexOrgans
- 62. Erection • Results fromblood flow into erectile tissues of the penis: – Corpora cavernosa and corpus spongiosum • Due to parasympathetic nerve−induced vasodilation of the arterioles leading to the corpora cavernosa
- 63. Erection – Nitric oxideserves as the neurotransmitter. • Activates guanylate cyclase to produce cGMP → Closes Ca2+ channels → Decreases cytoplasmic Ca2+ levels → Relaxes muscles – Venous outflow of blood is partially blocked during an erection.
- 64. Nitric Oxide andErection
- 65. Control of theErection • Controlled by the hypothalamus and the sacral region of the spinal cord – Can occur due to conscious sexual thought (hypothalamus → spinal cord → penis) or sensory stimulation (penis → spinal cord → penis)
- 66. Erectile Tissues ofthe Penis
- 67. Emission and Ejaculation •Emission is the movement of semen into the urethra. • Ejaculation is the forceful expulsion of semen from the urethra. – Both are under sympathetic nervous system control. – Contraction of smooth muscles in the tubules, seminal vesicle, prostate, and muscles at base of penis is involved in ejaculation.
- 68. Male Fertility • Asperm count < 20 million/ml semen is called oligospermia and is considered less fertile. – May be caused by heat, drugs, or anabolic steroids
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- 70. Vasectomy • Most widelyused and reliable form of male contraception – The vas deferens is cut and tied to prohibit sperm transport. – A vasectomy does not affect testosterone production or ejaculation.
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