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Maintenance of long-term potentiation in perforant path-granule cell synapses is accompanied by increased glutamate release. Here we investigate the role of synaptophysin in release and in expression of long-term potentiation in dentate gyrus. We report that long-term potentiation was accompanied by increased endogenous glutamate release and increased tyrosine phosphorylation of synaptophysin, but these changes were attenuated when long-term potentiation was inhibited by the tyrosine kinase inhibitor tyrphostin AG879 or by the NMDA antagonist D-aminophosphonovalerate. In vitro analysis revealed that KCl-induced glutamate release was abolished in synaptosomes prepared in the presence of antisynaptophysin. The data suggest a role for synaptophysin in release and indicate that activation of tyrosine kinase and synaptophysin phosphorylation contribute to long-term potentiation perhaps by modulating glutamate release.

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