Reproduction 11 Flashcards
Define gonads, gametes and germ cell
Gonads = the organ that prodcues gametes (ovary or testes)
Gametes = mature male or female reproductive cell with a haploid number of chromosomes
Germ cell = sperm or oocyte in their developmental precursors
Describe early gonad development
Same for both sexes
Three waves of increasing cells lead to the development of the gonads:
Primordial germ cells (PGC) form gametes; visible at the epithelium of yolk sac and migrate to genbital ridges,
Coelomic epithelium- sex chords, proliferate and penartrate deeply.
Mesonephric cells- blood vessels, form vasulature
Coelomic epithelium express SRY which form sertoli cells in testes. Within testes SRY is no longer epxressed due to testes producing own hormones
Describe the formation of the gonads
Indifferent until week 7 Primordial germ cells- diploid germ cell precursors that arise during gastrulation, derived from the epiblast
After week 3 proliferate by mitosis, migrate through amoeboid movement (guided by chemotaxis) to the region of the dorsal wall that will form the gonads
Describe ovarian development from week 7
Absence of SRY expression and Y chromosome female gonads develop, normal xx genotype germ cells
Not dependent on endocrine activity
In ovary, sex cord cells do not penartrate deeply, they cluter around PGC
Meonephric cells form vasulature
Describe the formation of the internal reproductive system
Week 7 onwards Gonads have a bipotent structure Male- Sex determining region Y gene (SRY)/ Testis determining factor (TDF) Columns of cells from the coelomic epithelium-proliferate and penetrate deep into the medullary mesenchyme to form the primitive sex cords–> express SRY–> become sertoli cells Sex chord cells surround the migrated primordial germ cells and to form the seminiferous tubules Migratory cells from the mesonephric primordia for the vasculature and leydig cells Female- default pathway, no endocrine influence, further development depends on the presence of normal germ cells (Turner’s syndrome (X0)–> oocyte death–> ovarian dysgenesis) Weeks 8-12 Two separate unipotent structures Wolffian Ducts (mesonephric)- Male Mullerian (paramesonephric)- female Males- Leydig cells produce androgen to maintain the Wolffian ducts and the Sertoli cells produce Mullerian Inhibitory substance (MIS) to cause the regression of the Mullerian Ducts Females- default pathway
Describe the formation of the external genitalia
Undifferentiated- Genital tubercle (Penis or clitoris), urogenital fold (urethra or labia minora), Labio-scrotal swelling (Scrotal sac or labia majora) Dihydrotestosterone from fetal testes promotes male development
External genitalia process
Gonads form either male or female strucure (bipotent strucutre)
In interal reproductvie system there are 2 separate unipotent structures:
MALE = Wolffian duct
FEMALE = Mullerian duct
In males Androgens (Leydig) maintain wolffian ducts forming epidiymis/vas deferens. Mullerian inhibitory substance (MIS) (Sertoli cells) casues regression of mullerian ducts so the female system cannot form.
Genital tubercle form penis, uro genital fold form spongy urethra
In females, there are no andrgoens so the wolffian duct will be lost and as no mullerian inhibitory substance, the mullerain duct can form
Genital tubercle forms clitoris, urogenital fold forms labia minora
Define the start of puberty
Menarche (first period) in females at around 12.9yrs (decreased from 17ys in the 1840s, but weight constant at around 47kg- patients with mutations in leptin (white adipocytes) fail to enter puberty, leptin receptor in hypothalamus, trigger or permissive?)
First ejaculation in males around 13.4 yrs
Both Followed by growth spurt, activation of the HPG axis, secondary sexual characteristics and reproductive maturity
Describe neuroendocrine control of puberty
Gonadotrophin releasing hormone (GnRH)- peptide hormone, stimulates release of gonadotrophins from anterior pituitary. gonadal activation is triggered by pulsitile release of GnRH (continuous release causes down-regulation of the receptor on the gonadothroph cells)
Kisspeptin 1 is associated with GnRH pulse generation- Kisspeptin-expressing neurones are intimately associated with GnRH-secreting neurones, kisspeptin pulses match GnRH pulse, kisspeptin expression rises at puberty, exogenous kisspeptin administration induces puberty
KNDy (Kisspeptin-facilliates, Neurokinin B- facilliates, Dysnorphin A- inhibits) Neurones–> GnRH neurones in the hypothalamus
What are gonadotrophins
Glyco proteins tht bind to recptors on the cells surface and signal via G proteins.
Control HPG axis (FSH and LH)
LH= acts on leydig, theca and granulosa cells
FSH = acts on sertoli and granulosa cells
hCG = acts on luteal cells
Describe the sex steroids
Progestagens (pregnacy) 3 different versions that bind to 2 receptors , androgens (maleness) 4 different androgens that bind to 1 recpetor and oestrogens (femaleness) 3 different versions that bind to 2 different receptorss - depending at what poit a female is in her life, is a different oestrogen (oestradiol, oestriol, oestrone)
Formation = Hypothalamus produces GnRH acts on pituiary by the GnRH receptor, leading to the production of FSH and LH. FSH acts on both males (sertoli cells) and females ( cummulus cells). LH acts on males (leydig cells) and females (theca cells). Both lead to the production of sex steriods. Kisspeptin regulaes the GnRH pulses, lectin is also involved.
Describe secondary sexual characteristics
Measured on the Tanner (timing stages) stages
Girls- ovarian oestrogen–> growth of breasts, and genitalian avarian and adrenal androgens–> pubic and axillary hair
Boys- testicular androgens–> growth of pubic, facial and axillary hair, genitalia, enlargement of larynx and laryngeal muscles
Describe the growth spurt
Last 24-36 months
Girls grow around 25cm, boys grow 28cm (boys start later and so start height is roughly 10cm more)
Growth hormone (GH) from the anterior pituitary stimulates production of IGF-1 (made in liver and locally by chondrocytes), which directly stimulates chondrocyte proliferation in the epiphyseal growth plate of bones
Higher levels oestrogen in late puberty cause fusion of the epiphyseal growth plates, cartilage entirely replaced with bone causing statural growth ceases
