The ovulation of a dominant follicle at the end of the follicular phase of the menstrual cycle is a result of endocrine signaling. During the luteal phase of a non-pregnant menstrual cycle, the corpus luteum dies and follicles are recruited to begin the next cycle. In the late follicular phase (days 8-14), a dominant follicle develops and a follicle ruptures, leading to the release of a cumulus-oocyte complex. This is facilitated by signaling from gonadotropes, GnRH neurons, and kisspeptin neurons. The levels of estrogen (E2) are high during this phase.

In the early follicular phase (days 3-7), large antral follicles are recruited by follicle-stimulating hormone (FSH). The levels of FSH decrease, while the levels of luteinizing hormone (LH) increase. The levels of progesterone (P4) are low, and there is no significant change in inhibin levels. 

During the late luteal phase (days 25-28), the corpus luteum from the ovulated dominant follicle dies, leading to a decrease in estrogen and progesterone levels. If there is no implantation, there is no rescue by human chorionic gonadotropin (hCG). The levels of FSH increase, leading to the recruitment of large antral follicles for the start of a new cycle. The corpus luteum progressively becomes less sensitive to basal LH and eventually dies if there is no increase in LH-like activity. 

In the luteal phase, the levels of estrogen and inhibin are high, while the levels of FSH and LH return to basal levels. The corpus luteum produces high levels of progesterone, along with estrogen and inhibin. The decline in FSH levels causes atresia of all but one follicle, leading to the selection of a dominant follicle that produces high levels of estrogen. The levels of estrogen and inhibin negatively feedback on FSH.

The pituitary gland responds to the decrease in estrogen and progesterone levels by increasing FSH secretion. High levels of estrogen have a positive feedback on gonadotropes, resulting in LH (and some FSH) surges. The high levels of progesterone, estrogen, and inhibin negatively feedback on LH and FSH, returning them to basal levels.

The human menstrual cycle involves a "dialogue" between the ovary and the pituitary gonadotropes. The changes in estrogen and inhibin levels are shown by the same line in the cycle.
808 SECTION8Berne & Levy Physiology •Fig. 44.23 A,Endocrinesignalingleadingtotheovulationofadominantfollicleattheendofthefollicularphaseofthemenstrualcycle.B,Endocrinesignalingduringthelutealphaseofanon-pregnantmenstrualcycleleadingtothedeathofthecorpusluteumandrecruitmentoffolliclestobeginnextcycle.LATE FOLLICULAR d8-14 EARLY FOLLICULAR d3-7 Dominant follicle COC Ruptured follicle Growing large antral follicles recruited by FSH Decreasing FSH basal LH (–)(–)(+)(+)High E2 no P4 Gonado-tropes GnRH neurons GnRH neurons Kisspeptin neurons Kisspeptin neurons Moderate E2 & inhibin no P4 LH surge @ midcycle GnRH rapid pulses Gonado-tropes GnRH slow pulses • Increasing (–) feedback causing lower FSH • Follicular atresia • Selection of dominant follicle Switch to (+) feedback-especially at level of pituitary sensitivity to rapid GnRH pulses • Meiotic maturation • Luteinization • Ovulation of cumulus-oocyte complex (COC) A. Follicular Phase LATE LUTEAL (d25-28) MID-LUTEAL (d17-24) Corpus luteum from ovulated dominant follicle Large antral recruitable follicles Dying corpus luteum (corpus albicans) If no implantation no rescue by hCG Maintains active corpus luteum FSH recruits large antral follicles new cycle starts Loss of negative feedack from ovary after corpus luteum dies Gonado-tropes GnRH neurons Kisspeptin neurons GnRH rapid pulses Gonado-tropes GnRH neurons Kisspeptin neurons GnRH slow pulses (–)(–)High P4 moderate & inhibition FSH Peak Basal LH & FSH No E2 inhibin or P4 B. Luteal Phase
CHAPTER 44 The Male and Female Reproductive Systems 809 1. Corpus luteum dies, E and P levels fall. 5. Declining FSH levels progressively cause atresia of all but 1 follicle – leading to selection of dominant follicle, which produces high levels of E. 9. The corpus luteum progressively becomes less sensitive to basal LH – dies if levels of LH-like activity (i.e., hCG) do not increase. 3. FSH recruits a cohort of large antral follicles to enter rapid growth phase. Follicles secrete low amounts of E and inhibin. 7. LH surge induces meiotic maturation, ovulation and luteinization. The corpus luteum produces high P, along with E and inhibin.
4. E and inhibin negatively feed back on FSH. FSH LH Pituitary
Progesterone OvaryEstradiol-17˜2. Pituitary responds to falling E and P by increasing FSH secretion. 6. High E has positive feedback on gonadotropes— LH (and some FSH) surges. 8. High P, E and inhibin negatively feed back on LH and FSH, returning them to basal levels.
•Fig. 44.24 Thehumanmenstrualcycle,withemphasisonthe“dialogue”betweenovaryandpituitarygonadotropes.NotethattherelativechangesinthelevelsofE2andinhibinareshownbythesameline.