Combined with feedback signals provided by E2 and progesterone (P), GnRH and Dop control synthesis and release of FSH, LH, and PRL. The production of the gonadotropins LH and FSH is stimulated by the GnRH signals and inhibited by the instantaneous levels of free E2 and P in the tissue. This model treats the LH and FSH signals to the ovaries as continuous serum levels.

The preovulatory gonadotropin surge, necessary for follicle growth and ovulation, is induced by an increase in circulating E2 concentrations that stimulates the secretion of GnRH from the hypothalamus as described before [70,71] and enhances pituitary responsiveness to GnRH [72,73]. This sudden rise in circulating LH and FSH levels is modeled by amplifying the GnRH signal.

The production of PRL by the lactotropic cells is inhibited by Dop, the inhibitory effects of which are blocked by E2 [74]. So when the free E2 concentration in the model exceeds a critical value, the inhibition of Dop is turned off for as long as the E2 level is elevated. The decreasing responsiveness of the pituitary gonadotropic membrane receptors [75] is modeled as a linear function of cumulative E2 exposure.

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