Abstract
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. The pharmacological profile was independent of AMPA receptors or the GluR5 subunit, indicating a possible role for the GluR6 subunit. KAR inhibition of I(sAHP) did not require ionotropic action or network activity, but was blocked by the inhibitor of pertussis toxin-sensitive G proteins, N-ethylmaleimide (NEM), or the PKC inhibitor calphostin C. These data suggest how KARs, putatively containing GluR6, directly increase excitability of CA1 pyramidal cells and help explain the propensity for seizure activity following KAR activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Action Potentials / physiology
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Animals
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Dose-Response Relationship, Drug
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Excitatory Amino Acid Agonists / pharmacology
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GluK2 Kainate Receptor
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Kainic Acid / pharmacology
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Potassium Channels, Inwardly Rectifying / antagonists & inhibitors
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Potassium Channels, Inwardly Rectifying / physiology*
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Protein Kinase C / antagonists & inhibitors
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiology*
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Rats
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Receptors, Kainic Acid / agonists
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Receptors, Kainic Acid / antagonists & inhibitors
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Receptors, Kainic Acid / physiology*
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Receptors, Metabotropic Glutamate / agonists
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Receptors, Metabotropic Glutamate / antagonists & inhibitors
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Receptors, Metabotropic Glutamate / physiology*
Substances
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Excitatory Amino Acid Agonists
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Potassium Channels, Inwardly Rectifying
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Receptors, Kainic Acid
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Receptors, Metabotropic Glutamate
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Protein Kinase C
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Kainic Acid