Luteinizing hormone causes granulosa cells to differentiate to form the corpus luteum and stimulates the corpus luteum to secrete hormones. Estrogens promote growth and function of the reproductive tract and stimulate proliferation of the endometrial lining. Estrogens also promote growth of the mammary glands. Progesterone promotes endometrial differentiation and, in conjunction with estrodiol, promotes mammary growth. Loss of estrogen and progesterone when the corpus luteum regresses results in shedding of the endometrial lining that was built up and sustained by these hormones (menstruation). Secretion of FSH and LH is stimulated by intermittent release of gonadotropin-releasing hormone (GnRH) by neurons in the arcuate nuclei of the hypothalamus. Secretion of FSH and LH during the follicular and luteal phases of the cycle is restrained by the negative feedback effects of ovarian hormones (negative feedback).
• Growth in the number and secretory capacity of granulosa cells during the follicular phase results in increasing blood concentrations of estradiol, which, upon reaching sustained high levels, triggers release of the ovulatory burst of LH and FSH (positive feedback).
• Negative feedback effects of progesterone on the hypothalamus slow the frequency of GnRH pulses and, on the pituitary, block the estrogen-induced surge of gonadotropin secretion.
• Both negative and positive feedback effects of estradiol are exerted primarily on the pituitary and can occur without a change in the pattern of GnRH secretion, but GnRH pulses increase in magnitude coincident with release of the ovulatory burst of gonadotropin secretion.
• Cues for timing critical events in the menstrual cycle arise in the ovary.
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