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Theoretically, the most effective inhibitory control of hypophysiotropic luteinizing hormone-releasing hormone (LHRH) release might occur through a presynaptic inhibition of LHRH neuronal terminals at the median eminence (ME) level. Since: (a) we have recently reported the existence of synaptic contacts between dopamine- and LHRH-containing processes in the ewe ME, and (b) nutritional deprivation induces an ovulatory failure in both birds and mammals, we have assessed the possibility that the anovulatory state induced by feed withdrawal (FW) in laying hens, might be caused by a dopaminergic inhibition of LHRH release at the ME level. Laying hens at the start (35 weeks old) and end (75 weeks old) of their commercial egg-laying life were killed at 0, 1, 2 and 4 days after FW. Serum luteinizing hormone (LH) and progesterone (P4), in vitro release of LHRH by isolated ME, and LHRH content in ME and preoptic area (POA) were determined by RIA. ME content of dopamine (DA) and its main metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) were assessed by LCED. The distribution of LHRH and tyrosine hydroxylase (TH)-containing processes at the ME level of the hen was determined immunocytochemically. In the hen, LHRH-containing cell bodies are localized in the anterior hypothalamus and medial POA. LHRH-containing axons project toward the ME and infundibulum through the ventral-lateral hypothalamus. TH-containing perikarya are concentrated in the arcuate nucleus and in the adjacent part of the periventricular nucleus, dorsal to the arcuate. TH-containing axons converge toward the ME and descend into the infundibulum. Dense concentrations of TH- and LHRH-containing processes are located in the lateral and mediobasal portions of the external layer of the ME, providing opportunities for synaptic interactions between them. Ovulatory failure and regression of the ovary and reproductive tract occurred 2-3 days after FW at the end, but not at the beginning of the hen's commercial egg-laying life. After FW, hens at the end of their productive life had higher (p less than 0.01) tuberoinfundibular DA turnover, produced less LHRH, and had lower serum LH and P4 than hens undergoing FW at the beginning of their productive life. In addition, in vitro release of HRH from denervated ME tissue of hens undergoing FW at the end of their commercial egg-laying life was higher and was reversed in a dose-dependent fashion by DA, but not by serotonin. Thus, the ovulatory failure associated with FW in laying hens might be caused by a presynaptic inhibition of in vivo LHRH release at the level of ME hypothalamic neuronal terminals.