Neuropeptides, the stress response, and the hypothalamo-pituitary-gonadal axis in the female rhesus monkey.
In conclusion, we have demonstrated that in the primate increased activity of the immune system and the consequent IL-1 release result in the activation of neuropeptides of the adrenal axis, mainly CRF and AVP. These neuropeptides, through a direct effect on the GnRH pulse generator or indirectly through the hypothalamic endogenous opioid peptides, inhibit the GnRH pulse generator. Some of the POMC derivatives, such as alpha-MSH, may antagonize these effects. The consequential decrease in GnRH pulse frequency results in an acute decrease in LH and FSH secretion. This decrease in gonadotropin release may explain the deleterious effects of stress on the menstrual cycle. However, an acute decrease in gonadotropins following activation of the adrenal axis is not observed in the presence of estradiol. Thus, during the menstrual cycle, a relative protection against the deleterious effects of acute stress may exist. How potent this protective mechanism is against repetitive stress is not known.
Ferin
M
M
Center for Reproductive Sciences, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000502:physiology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology*; D007109:Immunity; D008253:Macaca mulatta / Q000502:physiology*; D009479:Neuropeptides / Q000502:physiology*; D010053:Ovary / Q000502:physiology*; D010902:Pituitary Gland / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology*
D009479:Neuropeptides; D007987:Gonadotropin-Releasing Hormone; D003346:Corticotropin-Releasing Hormone