Absence of an effect of naloxone, an opioid antagonist, on luteinizing hormone release in vivo and luteinizing hormone-releasing hormone I release in vitro in intact, castrated, and food restricted cockerels.

The possibility that the tonic secretion of luteinizing hormone (LH) and chicken luteinizing hormone-releasing hormone I (LHRH-I) is regulated by an inhibitory action of endogenous opioid peptides was investigated in cockerels using the opiate receptor antagonist, naloxone. Baseline concentrations of plasma LH in the experimental cockerels were increased by surgical castration or reduced by limiting food intake. Baseline and K(+)-induced releases of LHRH-I from perifused mediobasal-preoptic hypothalami from castrated cockerels were higher than those from hypothalami from intact cockerels. Similarly, baseline and K(+)-induced releases of LHRH-I from perifused mediobasal hypothalami from fully fed cockerels were higher than those from the hypothalami from fasting cockerels. Intravenous injections of 0.1, 1, or 10 mg naloxone/kg body weight failed to increase the concentration of plasma LH in castrated, intact, fully fed, or fasted cockerels. Perifusion of mediobasal-preoptic hypothalami from castrated or intact cockerels with 200 microM naloxone or mediobasal hypothalami from fully fed or fasted cockerels with 10 microM naloxone failed to stimulate the release of LHRH-I. These observations suggest in the cockerel that endogenous opioid peptides may not play an obligatory role in the inhibitory control of the tonic secretion of luteinizing hormone.