ABSTRACT
The concept of opiate involvement in the control of reproduction by the brain stems from clinical observations that female narcotic addicts suffer from severe menstrual cycle disorders and that morphine, a synthetic alkaloid, readily inhibited ovulation and the preovulatory release of gonadotropins. The gradual decrease of the opioid restraint augments the rate of adrenergic turnover and neuropeptide Y and luteinizing hormone-releasing hormone (LHRH) elaboration in the median eminence (ME) nerve terminals in preparation for the trigger for LHRH release during the critical period. The opioid-LHRH functional link appears to be confined to the preoptic-tuberal pathway, primarily in the medial preoptic area and ME-arcuate nucleus. The proposal of adrenergic mediation of endogenous opioid peptides effects on LHRH release failed to accommodate the findings that a drastic reduction in adrenergic inputs to the hypothalamus on a chronic basis did not impair normal ovulatory cycles in the rat.
