RELEASE OF PROSTAGLANDIN ES BY HYPOTHALAMIC TISSUE - EVIDENCE FOR THEIR INVOLVEMENT IN CATECHOLAMINE-INDUCED LUTEINIZING-HORMONE-RELEASING HORMONE-RELEASE

Medial basal hypothalamic (MBH) and median eminence (ME) fragments from male rats were incubated in Krebs-Ringer bicarbonate-glucose buffer, pH 7.4, at 37.degree. C and the prostaglandin Es (PGE) released into the medium were measured by RIA [radioimmunoassay]. Basal release of PGE by the ME was 5-6 times greater than that by the MBH. If the ME was not separated from the MBH, the release of PGE by the MBH-ME unit was similar to that of the MBH alone. In vivo treatment with indomethacin (Id; [1-(p-chlorobenzoyl)-5-methoxy-2-methylindole-3-acetic acid]) to inhibit PG synthesis (single s.c. injection, 2.5 mg/100 g BW [body wt], 24 h before) decreased the basal release of PGEs by MBH and ME by about 50%. In vitro addition of Id (100 .mu.M) almost completely suppressed basal release of PGE by both the MBH and ME. Basal release of LHRH [luteinizing hormone releasing hormone] by the ME was also significantly depressed by Id. Incubation of the tissues with norepinephrine (NE) at doses (6-600 .mu.M) which increased LHRH output also elicited PGE release. Although dopamine (DA) also released LHRH, it was less effective than NE in inducing PGE release. As reported earlier for LHRH, the quantity of PGE released by the ME in response to the catecholamines was greater than that released by the MBH. Incubation of ME with different concentrations of PGE2 evoked LHRH release; the maximal effect was observed with the 0.28-.mu.M dose. Only this dose stimulated LHRH release by the MBH. Incubation of MBH or ME with PGF2.alpha. (0.028-2.8 .mu.M) failed to induce LHRH release. In vitro suppression of PG synthesis with Id completely abolished the release of LHRH by the ME induced by DA or NE (60 .mu.M). Release of LHRH induced by PGE2 (2.8 .mu.M) was not affected by the inhibitor. DA and NE can stimulate PGE release by the MBH and, especially, by the ME and that PGE2 acts mainly at the ME to evoke LHRH release. The stimulatory effect of both catecholamines on LHRH release is probably mediated by prostaglandins and catecholamines and PGE2 can stimulate LHRH release by acting on the ME terminals of LHRH-secreting neurons.