Kainate receptors (KARs) mediate postsynaptic responses in CA3 pyramidal cells and CA1 interneurones in the hippocampus. In CA1 pyramidal cells knockout studies have inidcated the presence of functional GluR6-containing KARs, however in this region they made no ionotropic contribution to the synaptic responses. In the meantime, a metabotropic function was reported for presynaptic KARs modulating transmitter release in CA1. We examined the possibility that KARs in CA1 pyramidal cells have a metabotropic function. Kainate is known to inhibit a slow afterhyperpolarization current that regulates excitability in hippocampus and can be modulated by a number of G protein coupled receptors. We showed that KARs activation reduces slow afterhyperpolarization current in CA1 pyramidal cells via metabotropic action and elucidated the transduction mechanism(s) underlying this action.
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