Prostaglandin E2-Induced Luteinizing Hormone- Releasing Hormone Release Involves Mobilization of Intracellular Ca+2*

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Abstract
In vitro experiments were performed to examine the involvement of Ca+2 in the mechanism by which prostaglandin E2 (PGE2) induces LHRH release from the median eminence (ME) of the hypothalamus [rat] Stepwise decreases in the Ca+2 concentration of the incubation medium reduced the LHRH response to PGE2. Nevertheless, neither complete omission of Ca+2 (residual Ca+2 concentration, 3.5 .mu.M) nor chelation of residual Ca+2 with EGTA [ethylene glycol bis(.beta.-aminoethyl ether) N,N,N'',N''-tetraacetic acid] prevented the stimulatory effect of the PG, suggesting that a significant portion of the PGE2 effect on LHRH release is independent of extracellular Ca+2. Blockade of Ca+2 influx with verapamil a Ca+2 entry blocker, demonstrated that this component of the PGE2 effect is completely independnet of inward Ca+2movement. Depletion of intraterminal Ca+2 stores by exposure of the MEs to the Ca+2 ionophore A23187 [calcimycin] in medium without Ca+2 containing EGTA almost completely obliterated the subsequent LHRH response to PGE2 indicating that normal inratermainal Ca+2 levels are important for the PGE2 effect to occur. Preloading the ME terminals with 45Ca+2 and subsequent stimulation with PGE2 demonstrated that even in the absence of extracellular Ca+2, PGE2 stimulates Ca+2 efflux from the terminals; this Ca+2 movement occurs temporarily associated with LHRH release. Depolarization of ME terminals with 56 mM K+ in the presence of normal Ca+2 concentration resulted in massive efflux of 45Ca+2 and a greater LHRH response than that produced by PGE2, suggesting that the effect fo PGE2 is not the consequence of a nonspecific general depolarization of ME nerve terminals. Although a full LHRH response to (exogenous) PGE2 necessitates normal extraterminal Ca+2 from intracellular stores apparently is an event involved in the mechansim by which PGE2 releases LHRH.

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