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Endocrinology, Vol 126, 1036-1042, Copyright © 1990 by Endocrine Society
ARTICLES |
R Medhamurthy, VL Gay and TM Plant
Department of Physiology, University of Pittsburgh School of Medicine, Pennsylvania 15261.
To examine the possibility that the prepubertal hiatus in gonadotropin secretion in primates is occasioned by an endogenous opioid peptide (EOP)-dependent suppression of pulsatile GnRH release, the ability of an EOP receptor antagonist, naloxone (NAL), to elicit GnRH release was examined indirectly in the rhesus monkey. For this purpose, six castrated male monkeys, aged 18-24 months, first received an intermitten iv infusion of GnRH (0.1 micrograms/min for 3 min every h) to enhance the responsiveness of the gonadotroph to endogenous GnRH. Acute and chronic blockade of EOP receptors with single bolus injections of NAL at three doses (0.2, 2.0, and 10 mg/kg BW) and a continuous infusion of the antagonist (2 mg/h for 36 h), respectively, failed to elicit significant increments in circulating concentrations of mean LH. In addition, changes in plasma LH concentrations during a chronic intermitten iv infusion of NAL (2 mg/kg BW every 6 h for up to 16 days) were unremarkable. Unequivocal discharges of LH, however, were observed in response to small doses of GnRH (0.3 micrograms/monkey) administered iv after all modes of NAL administration. Taken together, these findings fail to provide evidence for the view that in primates, EOPs underlie the hiatus in pulsatile GnRH release, which in these species is responsible for the quiescence of the pituitary-testicular axis during the greater part of prepubertal development.
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