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.

Protein kinase signalling requirements for metabotropic action of kainate receptors in rat CA1 pyramidal neurones.

Hippocampal pyramidal neurones display a Ca(2+)-dependent K(+) current responsible for the slow afterhyperpolarization (I(sAHP)), a prominent regulator of excitability. There is considerable transmitter convergence onto I(sAHP) but little information about the interplay between the kinase-based transduction mechanisms underlying transmitter action. We have added to existing information about the role of protein kinase C (PKC) in kainate receptor actions by demonstrating that direct postsynaptic activation of PKC with either 1-oleoyl-2-acethylsn-glycerol (OAG) or indolactam is sufficient to inhibit I(sAHP).

Role of protein kinase C in modulation of excitability of CA1 pyramidal neurons in the rat.

Biochemical and in situ hybridization studies demonstrated that the levels of protein kinase C variants were significantly increased in the hippocampus of the experimental models of epilepsy in rats. In addition it has been demonstrated that protein kinase C plays an important role in modulating synaptic transmission in the hippocampus. We examined the effects of activating of protein kinase C on the excitability of CA1 pyramidal neurons and synaptic transmission, using whole-cell current-clamp and extracellular field potential recording techniques.

Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors.

Prolonged modification of intrinsic neuronal excitability is gaining prominence as an activity-dependent form of plasticity. Here we describe a potential synaptic initiation mechanism for these changes in which release of the transmitter glutamate acts on kainate receptors to regulate the postspike slow afterhyperpolarization (sAHP). This action of synaptically released glutamate was occluded by previous kainate application.

Metabotropic-mediated kainate receptor regulation of IsAHP and excitability in pyramidal cells.

Kainate receptors (KARs) on CA1 pyramidal cells make no detectable contribution to EPSCs. We report that these receptors have a metabotropic function, as shown previously for CA1 interneurons. Brief kainate exposure caused long-lasting inhibition of a postspike potassium current (I(sAHP)) in CA1 pyramidal cells.