Effect of stress on the activity of the hypothalamic-pituitary-gonadal axis: peripheral and central mechanisms.
This article reviews the mechanisms believed to mediate stress-induced inhibition of reproductive functions and the anatomical sites at which these effects take place. Particular emphasis is placed on the potential modulating role of hormones or neurotransmitters released during stress. At the level of the gonads, adrenal corticoids, pro-opiomelanocortin (POMC)-like peptides, and corticotropin-releasing factor (CRF) are reported to interfere with the stimulatory action of gonadotropins on sex steroid-producing cells. Increased circulating corticosteroid levels may also decrease pituitary responsiveness to GnRH. There is, however, increasing evidence that these mechanisms are primarily involved in mediating the effects of prolonged stress, but not those of an acute stimulus. In contrast, a variety of hormones or neurotransmitters, including CRF, POMC peptides, and biogenic amines act within the brain to mediate the inhibitory influence of both acute and prolonged stresses on reproductive function.
Rivier
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Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, California 92037.
Rivest
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D000305:Adrenal Cortex Hormones / Q000502:physiology; D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000502:physiology; D006062:Gonadotropins / Q000037:antagonists & inhibitors*; D006066:Gonads / Q000503:physiopathology*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D011333:Pro-Opiomelanocortin / Q000502:physiology; D013312:Stress, Physiological / Q000503:physiopathology*; D001615:beta-Endorphin / Q000502:physiology
D000305:Adrenal Cortex Hormones; D006062:Gonadotropins; D001615:beta-Endorphin; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone