Release of prostaglandin E2 from the hypothalamus depends on extracellular Ca2+ availability: Relation to LHRH release

Sergio Ojeda, Andres Negro-Vilar

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

The present experiments were performed to investigate the role of extracellular Ca2+ in the process of prostaglandin E2 (PGE2) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K+ induced a dose-related increase in PGE2 and LHRH release. The effect of K+ depended upon the Ca2+ concentration in the incubation medium. A Ca2+ concentration of 0.1 mM was sufficient to permit a significant response in both PGE2 and LHRH release to K+. The effect of a maximal K+ concentration (56 mM) was almost completely obliterated by omitting Ca2+ from the incubation medium and by chelating the remaining Ca2+ with EDTA or EGTA. The Ca2+ ionophore A23187, tested at different concentrations (1-50 μM) significantly increased the release of both PGE' and LHRH from the ME in a Ca2 + -dependent manner. A Ca2" concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE2 response. Blockade of Ca2+ channels with Verapamil, a Ca2+ entry blocker, prevented the effect of K+ on both PGE2 and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE: From ME nerve terminals depends upon the concentration of extracellular Ca2+ and suggest that PGE2 release is initiated by an increase in Ca2+ influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca2+ influx through Ca2+ voltage-dependent channels.

Original languageEnglish (US)
Pages (from-to)442-447
Number of pages6
JournalNeuroendocrinology
Volume39
Issue number5
StatePublished - 1984
Externally publishedYes

Fingerprint

Dinoprostone
Gonadotropin-Releasing Hormone
Hypothalamus
Median Eminence
Ionophores
Prostaglandins E
Median Nerve
Egtazic Acid
Calcimycin
Verapamil
Edetic Acid

Keywords

  • Extracellular Ca<sup>2+</sup>
  • LHRH
  • Median eminence
  • Prostaglandin E<inf>2</inf>

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems
  • Neuroscience(all)

Cite this

Release of prostaglandin E2 from the hypothalamus depends on extracellular Ca2+ availability : Relation to LHRH release. / Ojeda, Sergio; Negro-Vilar, Andres.

In: Neuroendocrinology, Vol. 39, No. 5, 1984, p. 442-447.

Research output: Contribution to journalArticle

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N2 - The present experiments were performed to investigate the role of extracellular Ca2+ in the process of prostaglandin E2 (PGE2) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K+ induced a dose-related increase in PGE2 and LHRH release. The effect of K+ depended upon the Ca2+ concentration in the incubation medium. A Ca2+ concentration of 0.1 mM was sufficient to permit a significant response in both PGE2 and LHRH release to K+. The effect of a maximal K+ concentration (56 mM) was almost completely obliterated by omitting Ca2+ from the incubation medium and by chelating the remaining Ca2+ with EDTA or EGTA. The Ca2+ ionophore A23187, tested at different concentrations (1-50 μM) significantly increased the release of both PGE' and LHRH from the ME in a Ca2 + -dependent manner. A Ca2" concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE2 response. Blockade of Ca2+ channels with Verapamil, a Ca2+ entry blocker, prevented the effect of K+ on both PGE2 and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE: From ME nerve terminals depends upon the concentration of extracellular Ca2+ and suggest that PGE2 release is initiated by an increase in Ca2+ influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca2+ influx through Ca2+ voltage-dependent channels.

AB - The present experiments were performed to investigate the role of extracellular Ca2+ in the process of prostaglandin E2 (PGE2) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K+ induced a dose-related increase in PGE2 and LHRH release. The effect of K+ depended upon the Ca2+ concentration in the incubation medium. A Ca2+ concentration of 0.1 mM was sufficient to permit a significant response in both PGE2 and LHRH release to K+. The effect of a maximal K+ concentration (56 mM) was almost completely obliterated by omitting Ca2+ from the incubation medium and by chelating the remaining Ca2+ with EDTA or EGTA. The Ca2+ ionophore A23187, tested at different concentrations (1-50 μM) significantly increased the release of both PGE' and LHRH from the ME in a Ca2 + -dependent manner. A Ca2" concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE2 response. Blockade of Ca2+ channels with Verapamil, a Ca2+ entry blocker, prevented the effect of K+ on both PGE2 and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE: From ME nerve terminals depends upon the concentration of extracellular Ca2+ and suggest that PGE2 release is initiated by an increase in Ca2+ influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca2+ influx through Ca2+ voltage-dependent channels.

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