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

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

Research output: Contribution to journalArticle

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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 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 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 PGF(2α) (0.028-2.8 μM) 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 μM). 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
StatePublished - 1979
Externally publishedYes

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Median Eminence
Gonadotropin-Releasing Hormone
Prostaglandins
Catecholamines
Norepinephrine
Dinoprostone
Dopamine
Prostaglandins F
Bicarbonates
Indomethacin
Acetic Acid

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Release of prostaglandin Es by hypothalamic tissue : Evidence for their involvement in catecholamine-induced luteinizing hormone-releasing hormone release. / Ojeda, Sergio; Negro-Vilar, A.; McCann, S. M.

In: Endocrinology, Vol. 104, No. 3, 1979, p. 617-624.

Research output: Contribution to journalArticle

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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 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 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 PGF(2α) (0.028-2.8 μM) 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 μM). 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.",
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AU - McCann, S. M.

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