It has been suggested that hypothalamic median eminence (ME) might be a control site for luteinizing hormone-releasing hormone (LHRH) release. Thus, stimulatory and/or inhibitory inputs acting at this site might be involved in regulating LHRH release from the ME and, therefore, luteinizing hormone (LH) release from the anterior pituitary. Since a role for neuropeptide Y (NPY) on LH release has been suggested, we hav hypothesized that NPY might act in the ME to control preovulatory LHRH release in hens. To examine this possibility we have detrmined: (a) the immunocytochemical distribution of LHRH and NPY in the ME of the hen, (b) the basal and NPY-stimulated release of LHRH in vitro from the ME of hens undergoing a natural or a premature preovulatory surge of LH, and (c) the tissue content of LHRH and NPY in microdissected MEs, at various times before and during a natural or a premature preovulatory surge of LH. A potential role for NPY on LHRH release in the ME is suggested for the following reasons, (a) There are opportunities for synaptic interactions between NPY and LHRH-containing axons at this site. LHRH-containing cell bodies localized in the anterior hypothalamus/medial preoptic area project to the ME. NPY-containing perikarya, concentrated in the ventromedial aspect of the arcuate nucleus, might contact LHRH processes going to the ME and/or might themselves send axons to the ME, (b) Addition of NPY to the incubation media increases LHRH release from microdissected ME tissue of hens killed at the time of the natural preovulatory surge of LH, but not in hens killed 7 h before the occurrence of this surge. However, the stimulatory effect of NPY on LHRH release can be induced at this latter time when a premature LH surge is elicited. While the natural preovulatory surge of LH occurs 4 h before the second ovulation in a sequence (C2 ovulation), administration of progesterone (P4) 10-14 h before the expected natural C2 ovulation advances the natural LH surge by 7-8 h. Thus, NPY might act as a physiological stimulus of LHRH release at the ME during the preovulatory surge of LH. This is suggested since in vitro basal LHRH release from denervated ME tissue does not change before and during the natural or the premature LH surge. Therefore, preovulatory release of LHRH in vivo might be under a continuous drive from stimulatory inputs to the LHRH neuron and NPY might be one of these stimulating factors, (c) An acute preovulatory decrease in ME-NPY tissue content is consistent with its putative role on preovulatory LHRH release. During both the natural and the premature preovulatory period, NPY content reaches nadir values at the time of the LH surge, which occurs 7-8 h earlier in the premature than in the natural model. In conclusion, NPY might be acting at the median eminence as a physiological stimulus for preovulatory LHRH release.
We studied the effect that β-endorphin (βEND) 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 βEND and LHRH in the hen ME, (b) the temporal changes in ME and preoptic area (POA) LHRH and βEND 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 βEND in both models, and (d) the effect of βEND and naloxone on in vitro ME-LHRH release in the two models. In the hen, βEND 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 βEND 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-βEND 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 βEND decreased: ME-βEND 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-βEND was also evident 1 h after P4. POA-LHRH content remained unchanged through the time period. On the other hand, basal in vitro ME-βEND 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, βEND 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 βEND that decreased in vitro ME-LHRH release in hens killed during their spontaneous LH surge were ineffective in hens killed during a premature LH surge. In conclusion, a transient decrease of a βEND 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.
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