Release of prostaglandin es by hypothalamic tissue:evidence for their involvement in catecholamine-induced luteinizing hormone-releasing hormone release

S. R. Ojeda, A. Negro-Vilar, S. M. McCann

    Research output: Contribution to journalArticle

    148 Scopus citations

    Abstract

    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 C and the prostaglandin Es (PGEs) released into the medium were measured by RIA. Basal release of PGE by the ME was 5-6 times greater than that by the MBH. However, if the ME was not separated from the MBH, the release of PGE by the MBHME unit was similar to that of the MBH alone. In vivo treatment with indomethacin (Id; [l-(p-chlorobenzoyl)-5-methoxy-2-methylindole 3-acetic acid]) to inhibit PG synthesis (single sc injection, 2.5 mg/100 g BW, 24 h before) decreased the basal release of PGEs by MBH and ME by about 50%. In vitro addition of Id (100 μM) almost completely suppressed basal release of PGEs by both the MBH and ME. Basal release of LHRH by the ME was also significantly depressed by Id. Incubation of the tissues with norepinephrine (NE) at doses (6-600 μM) 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 PGEs 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-μM dose. Only this dose stimulated LHRH release by the MBH. Incubation of MBH or ME with PGF2α (0.028-2.8 JUM) 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 fiM). However, release of LHRH induced by PGE2 (2.8 μM) was not affected by the inhibitor. The results indicate that DA and, particularly, 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. In addition, they suggest that 1) the stimulatory effect of both catecholamines on LHRH release is mediated by prostaglandins, and 2) catecholamines and PGE2 can stimulate LHRH release by acting on the ME terminals of LHRH-secreting neurons.

    Original languageEnglish (US)
    Pages (from-to)617-624
    Number of pages8
    JournalEndocrinology
    Volume104
    Issue number3
    DOIs
    StatePublished - Mar 1979

    ASJC Scopus subject areas

    • Endocrinology

    Fingerprint Dive into the research topics of 'Release of prostaglandin es by hypothalamic tissue:evidence for their involvement in catecholamine-induced luteinizing hormone-releasing hormone release'. Together they form a unique fingerprint.

  • Cite this