Circadian rhythm affects Pit releases Coticosteroids & PRL post Pituitary hormones

A glimpse on Pituitary gland & its hormones in reproduction:  We all owe to FSH & LH, PRL, TSH, Growth hormone, PRL, Corticosteroids The Ant Pit P is a gland distinct from the brain. The posterior pituitary (PP) is actually an extension of the brain - so PP secretions are Neurohormonal.

AP hormones are glandular hormones (not Neurohormonal). The hypothalamus (in the brain) secretes hormones into

the hypothalamic-hypophyseal portal veins. Most species have a distinct breeding season - reproduction shuts down for both sexes during parts of the year in which resources are limited. Breeding is timed so that young are growing fastest when resources are most abundant. Within the breeding season, the endocrine control of reproduction in males and females is very different - males are continuously fertile, but females ovulate cyclically. Control of ovulation is complex. Could start the description at several places - arbitrarily, I'll begin with ovary and follicles, and work up from there.  Even before a female is born, her ovaries hold ova (eggs, female gametes). In animmature female, each egg is enclosed in a primary follicle (small, no membrane). Most eggs in an adult female are also in primary follicles. At any time, a small subset develop into secondary follicles (larger, surrounded by membrane). \

In each estrous cycle, large secondary follicles are recruited to become Graafian follicles. Mature, Graafian follicles have a fluid filled cavity (the antrum). The egg itself projects into this space, surrounded by granulosa cells, which primarily secrete estrogen. The projection into the antrum is called the cumulus oophorus. A 'ripe' follicle moves up to the surface of the ovary so that it bulges out, with the cumulus oophorus on the side away from the ovarian wall. A site (the stigma) develops on the outer surface, where the tissue changes so that the follicle can rupture. At ovulation, the follicle splits and the eggshoots out with the antral fluid. Many secondary and Graafian follicles regress without ovulating (called atresia). This is not well understood, but it is normal after ovulating, the follicle fills with blood and lymph. The blood clot is resorbed as luteinization occurs, and is replaced by granulosa cells that form a corpus luteum (CL,'dark body' plural = corpora lutea). These cells primarily secrete progesterone.  After a period (usually a few days to a few weeks, but longer in some species), the CL.regresses, progesterone secretion drops, and it converts to a non-functional corpus albicantia ('white body') made mostly of connective tissue - eventually becomes barely detectable scar on surface of ovary. Endocrine control of ovarian cycles: Follicular phase: prior to ovulation, cells in the follicle primarily secrete estrogen. Luteal phase: after ovulation, cells in the corpus luteum primarily secrete progesterone, but also secrete some estrogen.Some shorthand - most of the estrogen is estradiol - E2 Progesterone - P4.. Noted before that there are many follicles in ovary. After an ovulation, the CL's from that ovulation secrete P4. But other pre-ovulatory follicle are growing, and they secrete E2.Result - the ratio of E2/P4 varies through time.

•         E₂:P₄ increases as follicle grows

•         E₂:P₄ drops abruptly at ovulation

•         E2:P4 increases as CL's regress

Variation in E2:P4 ratio is important in understanding how endocrine feedback loops control ovulation.

Higher levels controlling folliculogenesis and ovulation. Hypothalamus controls anterior pituitary (AP), which controls ovary.

 (Diagram of loops: GnRH, gonadotropins (FSH and LH), ovarian steroids (estrogen and progesterone).

Sequence of events:

1.       Hypothalamus secretes Gonadotropin Releasing Hormone (GnRH).

2.       GnRH stimulates secretion of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) by the AP. (always a + effect).

3.       FSH stimulates growth of pre-ovulatory follicles(s).

4.       As follicles grow, they secrete estrogen in increasing amounts. Two endocrine steps here -

LH stimulates ovary (thecal cells, outside follicle) to secrete testosterone.

FSH stimulates conversion of androgen to estradiol (granulosa cells, in follicle).

5.       LH and FSH feedback negatively on the secretion of GnRH by the hypothalamus. This helps to terminate the stimulation of follicles to grow.

6.       Estrogen and progesterone normally feedback negatively on the hypothalamus and AP. But as E2:P4 ratio increases, the feedback becomes positive.

7.       Note that the follicle is growing with constant level of FSH. It is an increase in sensitivity of ovary to FSH that causes follicular growth, initially.

8.       As E2 increases (b/c ovary is growing) E2:P4 ratio increases and feedback of estrogen on hypothalamus and AP switches to positive feedback.

9.       Shift to positive feedback causes estrogen surge.

10.   Estrogen surge, with positive feedback, causes ovulatory pulse of LH.

11.   LH pulse causes ovulation.

12.   Follicle becomes CL and secretes much more P4 than previously (but also secretes estrogens).

13.   Drop in E2 causes LH to return to baseline. If non-conceptive, FSH also drops to baseline. Feedback of steroids on AP and hypothalamus switches back to negative. Inhibin, an ovarian peptide hormone, also contributes to negative feedback.

CL collapses to become (nonsecretory) corpus albicantia after a period that varies among species. Prostaglandins, especially PGF2a, contribute to regression of CL (luteolysis). PGF2a may have multiple sources, but uterine