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1 Laboratory of Cellular and Synaptic Neurophysiology, NICHD, NIH, Bethesda, MD 20892, USA
2
Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA 92037, USA
3
Nobel Institute for Neurophysiology, Department of Neuroscience, Retzius väg 8, A3:5, Karolinska Institute, SE-17177 Stockholm, Sweden
Abstract
Kainate receptors (KARs) play an important role in synaptic physiology, plasticity and pathological phenomena such as epilepsy. However, the physiological implications for single cells and neuronal networks of the distinct expression patterns of KAR subunits are unknown. One intriguing effect of KAR activation is a long-term change to intrinsic neuronal excitability and neuronal firing patterns, such as single-spike and spike-burst firing. In this study, we describe the role of kainate receptor subunits in the metabotropic regulation of the slow and medium afterhyperpolarization (AHP) currents (IsAHP, ImAHP). Using whole-cell patch-clamp recordings from CA3 pyramidal cells of wild-type (WT) and KAR knockout mice, we show that the kainate-induced decrease of IsAHP and ImAHP amplitude is protein-kinase-C-dependent and absent in GluR6–/– but not GluR5–/– pyramidal neurones. Our findings suggest that activation of GluR6-containing KARs modulates AHP amplitude, and influences the firing frequency of pyramidal neurones.
(Received 14 October 2004;
accepted after revision 5 November 2004;
first published online 11 November 2004)
Corresponding author A. Fisahn: Nobel Institute for Neurophysiology, Department of Neuroscience, Retzius väg 8, A3:5, Karolinska Institute, SE-17177 Stockholm, Sweden. Email: andre.fisahn{at}neuro.ki.se
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