Metabotropic actions of kainate receptors in the regulation of I(sAHP) and excitability in CA1 pyramidal cells.

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.