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Journal of Clinical Endocrinology & Metabolism, Vol 66, 722-726, Copyright © 1988 by Endocrine Society
ARTICLES |
RM Sapolsky and LC Krey
Department of Biological Sciences, Stanford University, California 94305.
Numerous stressors disrupt male reproductive physiology; previous studies of a population of wild baboons, living freely in a national park in East Africa, indicated that the stress of anesthetization by phencyclidine darting decreased both LH secretion and testicular sensitivity to LH. This study was undertaken to determine the mechanism(s) of the decreased LH secretion in these animals. Neither stress-induced glucocorticoid nor catecholamine release was responsible, since neither blockade of glucocorticoid secretion with the adrenal steroidogenesis inhibitor metyrapone nor blockade of catecholamine secretion with the sympathetic ganglionic blocking drug chlorisondamine prevented the stress-induced decline in serum LH concentrations. Administration of the opiate receptor antagonist naloxone (0.5 mg/kg BW), however, not only prevented the decline, but also transiently elevated serum LH concentrations, suggesting that opiates play a role in tonic as well as stress-induced decreases in LH secretion. Administration of a small dose of naloxone (0.03 mg/kg BW) commensurate with occupancy of only mu-opiate receptors slowed the stress-induced decline in LH concentrations, as did administration of the kappa-receptor antagonist MR 1452. These data suggest that opiates inhibit LH release via the combined occupancy of both mu- and kappa- receptors.
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