Kainate (KA) receptors (KARs) are important modulators of synaptic transmission. We studied here the role of KARs on glutamatergic synaptic transmission in the CA2 region of the hippocampus where the actions of these receptors are unknown. We observed that KA depresses glutamatergic synaptic transmission at Schaffer collateral-CA2 synapses; an effect that was antagonized by NBQX (a KA/AMPA receptors antagonist) under condition where AMPA receptors were previously blocked. The study of paired-pulse facilitation ratio, miniature responses and fluctuation analysis indicated a presynaptic locus of action for KAR. Additionally, we determined the action mechanism for this depression of glutamate release mediated by the activation of KARs. We found that inhibition of protein kinase A (PKA) suppressed the effect of KAR activation on eEPSC, an effect that was not suppressed by protein kinase C inhibitors. Furthermore, in the presence of Pertussis toxin, the depression of glutamate release mediated by KAR activation was not present, invoking the participation of a G protein in this modulation. Finally, the KAR-mediated depression of glutamate release was not suppressed by treatments that affect calcium entry trough voltage-dependent calcium channels or calcium release from intracellular stores. We conclude that KARs present at these synapses mediate a depression of glutamate release through a mechanism that involves the activation of G-protein and protein kinase A.
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