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      Release of Prostaglandin E 2 from the Hypothalamus Depends on Extracellular Ca 2+ Availability: Relation to LHRH Release



      S. Karger AG

      Prostaglandin E2 , LHRH, Extracellular Ca2+ , Median eminence

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          The present experiments were performed to investigate the role of extracellular Ca<sup>2+</sup> in the process of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) 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<sup>+</sup> induced a dose-related increase in PGE<sub>2</sub> and LHRH release. The effect of K<sup>+</sup> depended upon the Ca<sup>2+</sup> concentration in the incubation medium. A Ca<sup>2+</sup> concentration of 0.1 mM was sufficient to permit a significant response in both PGE<sub>2</sub> and LHRH release to K<sup>+</sup>. The effect of a maximal K<sup>+</sup> concentration (56 mM)was almost completely obliterated by omitting Ca<sup>2+</sup> from the incubation medium and by chelating the remaining Ca<sup>2+</sup> with EDTA or EGTA. The Ca<sup>2+</sup> ionophore A23187, tested at different concentrations (1–50 µ M) significantly increased the release of both PGE<sub>2</sub> and LHRH from the ME in a Ca<sup>2+</sup>-dependent manner. A Ca<sup>2+</sup> concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE<sub>2</sub> response. Blockade of Ca<sup>2+</sup> channels with Verapamil, a Ca<sup>2+</sup> entry blocker, prevented the effect of K<sup>+</sup> on both PGE<sub>2</sub> and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE<sub>2</sub> from ME nerve terminals depends upon the concentration of extracellular Ca<sup>2+</sup> and suggest that PGE<sub>2</sub> release is initiated by an increase in Ca<sup>2+</sup> influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca<sup>2+</sup> influx through Ca<sup>2+</sup> voltage-dependent channels.

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          Author and article information

          S. Karger AG
          28 March 2008
          : 39
          : 5
          : 442-447
          Department of Physiology, University of Texas Health Science Center, Dallas, Tex., USA
          124018 Neuroendocrinology 1984;39:442–447
          © 1984 S. Karger AG, Basel

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          Pages: 6
          Original Paper


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