Abstract
Kainate receptors (KARs) effect depression of glutamate release at hippocampal mossy fiber-CA3 (MF-CA3) synapses by a metabotropic action involving adenylyl cyclase (AC) inhibition, cAMP reduction, and diminished protein kinase A (PKA) activation. Using hippocampal slices, we show here that KAR activation interferes with the depression of glutamate release produced by Group II metabotropic glutamate receptor stimulation and low frequency stimulation (LFS)-induced long-term depression (LTD), also expressed through presynaptic AC/cAMP/PKA at MF-CA3 synapses. The mutual occlusion of depression mediated by presynaptic KARs, Group II mGluR and LFS-induced LTD suggests their mechanistic convergence at the MF-CA3 synapse and thus invokes KARs in synaptic plasticity manifest in LTD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cyclic AMP-Dependent Protein Kinases / physiology
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Data Interpretation, Statistical
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Electrophysiology
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / physiology
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In Vitro Techniques
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Kainic Acid / pharmacology
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Mice
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Mice, Inbred C57BL
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Mossy Fibers, Hippocampal / physiology*
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Neuronal Plasticity / physiology*
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Patch-Clamp Techniques
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Receptors, Kainic Acid / physiology*
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Receptors, Metabotropic Glutamate / physiology*
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Receptors, Presynaptic / physiology*
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Synapses / physiology*
Substances
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Excitatory Amino Acid Antagonists
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Receptors, Kainic Acid
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Receptors, Metabotropic Glutamate
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Receptors, Presynaptic
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metabotropic glutamate receptor 2
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Cyclic AMP-Dependent Protein Kinases
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Kainic Acid