BETA-ENDORPHIN REGULATION OF LHRH RELEASE AT THE MEDIAN-EMINENCE LEVEL - IMMUNOCYTOCHEMICAL AND PHYSIOLOGICAL EVIDENCE IN HENS

We studied the effect that beta-endorphin (betaEND) might have at the median eminence (ME) on luteinizing hormone (LH)-releasing hormone (LHRH) during the ovulatory cycle of domestic hens. Thus, we assessed (a) the immunocytochemical distribution of betaEND and LHRH in the hen ME, (b) the temporal changes in ME and preoptic area (POA) LHRH and betaEND content, in both a spontaneous and a premature C2 ovulatory model. The premature C2 ovulation occurs 6-7 h after the administration of progesterone (P4) injected 14 h before the spontaneous second (C2) ovulation of a sequence and therefore 7-8 h earlier than expected, (c) the ME in vitro release of betaEND in both models, and (d) the effect of betaEND and naloxone on in vitro ME-LHRH release in the two models. In the hen, betaEND cell bodies are located in the periarcuate area with axons projecting to both the ME and the POA. LHRH perikarya are located in the medial POA and anterior hypothalamus and project to the ME and infundibulum through the ventrolateral hypothalamus. In the spontaneous C2 ovulatory model, both betaEND and LHRH content in the ME remained unchanged during the 14 h preceding the C2 ovulation. However, POA-LHRH content was increasing at the time of the LH surge (4 h before the expected C2 ovulation) and remained elevated until the C2 ovulation occurred. In contrast, POA-betaEND content was lowest at the time of the LH surge and remained low until the C2 ovulation occurred. In the premature C2 ovulatory model, the ME content of both LHRH and betaEND decreased: ME-betaEND content declined at the time of the premature preovulatory LH release (3 h after P4 administration and 3 h prior to the premature ovulation) and ME-LHRH content declined 1 h after P4 injection. A reduction in POA-betaEND was also evident 1 h after P4. POA-LHRH content remained unchanged through the time period. On the other hand, basal in vitro ME-betaEND release decreased at the time of the spontaneous LH surge when compared to its basal release 7 h before. This decrease occurred 7 h earlier in the premature model, albeit somewhat attenuated, associated with the premature LH surge. Finally, betaEND inhibited and naloxone stimulated, both in a dose-dependent manner, in vitro ME-LHRH release at the time of the expected spontaneous LH surge. However, at the time of the premature LH surge, only the highest dose of naloxone increased in vitro ME-LHRH release, and this to a lesser extent than in hens undergoing a spontaneous LH surge. Similar doses of betaEND that decreased in vitro ME-LHRH release in hens killed dufing their spontaneous LH surge were ineffective in hens killed during a premature LH surge. In conclusion, a transient decrease of a betaEND inhibitory tone on LHRH neuronal terminals at the median eminence level might play a role in the release of LHRH at the time of the spontaneous preovulatory LH surge in the hen.