Modulation by endogenous opioid peptides of the secretion of LHRH from cockerel ( Gallus domesticus ) mediobasal hypothalamic tissue

An in-vitro superfusion system was used to study the effects of the endogenous opioid peptides [Met]-enkephalin (and its long-lasting analogue [D-Ala2,Met]-enkephalinamide), [Leu]-enkephalin and beta-endorphin and of the opiate antagonist naloxone, on the secretion of LHRH from the mediobasal hypothalamus of the cockerel. The effects of the compounds on both basal release of LHRH and on release stimulated by a depolarizing pulse of increased extracellular potassium ion (64 mmol/l) were investigated. None of the endogenous opioid peptides altered basal release of LHRH; however, both [Met]-enkephalin (10 mumol/l) and [D-Ala2,Met]-enkephalinamide (1 mumol/l) significantly (P less than 0.05) reduced the response to depolarization. Neither [Leu]-enkephalin nor beta-endorphin (0.1-10 mumol/l) were effective. Naloxone (1 mumol/l) administered alone significantly (P less than 0.05) increased basal release of LHRH and abolished the inhibitory effects of [Met]-enkephalin and [D-Ala2,Met]-enkephalinamide on depolarization-induced release. These results suggest that the endogenous opioid peptides exert a tonic inhibitory influence on LHRH secretion by the mediobasal hypothalamus of the cockerel.