Release of Prostaglandin E2 from the Hypothalamus Depends on Extracellular Ca2+ Availability: Relation to LHRH Release

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Abstract
The role of extracellular Ca2+ in the process of prostaglandin E2 (PGE2) release from the median eminence (ME) of the [rat] hypothalamus was investigated. 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 on 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 .mu.M) significantly increased the release of both PGE2 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. Release of PGE2 from ME nerve terminals evidently depends on the concentration of extracellular Ca2+. PGE2 release is initiated by an increase in Ca2+ influx to the terminals. Release of LHRH evidently is, to a significant extent, a function of Ca2+ influx through Ca2+ voltage-dependent channels.

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