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The Journal of Neuroscience, May 12, 2004, 24(19):4530-4534; doi:10.1523/JNEUROSCI.5356-03.2004

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BRIEF COMMUNICATION
Metabotropic Regulation of Intrinsic Excitability by Synaptic Activation of Kainate Receptors

Zare Melyan,¹ Barrie Lancaster,² and Howard V. Wheal¹

¹Neuroscience Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, United Kingdom, and ²Wolfson Institute for Biomedical Research, University College London, London WC1E 6BT, United Kingdom

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. Furthermore, inhibition of glutamate uptake enhanced the effects of synaptic activation. Glutamate-mediated kainate receptor inhibition of sAHP current (I_sAHP) was blocked by the PKC inhibitor calphostin C, confirming the requirement for a metabotropic signaling cascade. These data describe a new physiological function for glutamate release: activation of metabotropic kainate receptors, which control directly the excitability of pyramidal cells and probably contribute to prolonged excitability changes.

Key words: calphostin C; hippocampus; kainic acid; potassium channels; protein kinase C; pyramidal cells; kainate receptor

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Received Dec 4, 2003; revised March 17, 2004; accepted March 24, 2004.

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