Abstract
Kainate receptors (KARs) are a poorly understood family of ionotropic glutamate receptors. A role for these receptors in the presynaptic control of transmitter release has been proposed but remains controversial. Here, KAR agonists are shown to enhance fiber excitability, and a number of experiments show that this is a direct effect of KARs on the presynaptic fibers. In addition, KAR activation inhibits evoked transmitter release from mossy fiber synapses. Synaptic release of glutamate from either neighboring mossy fiber synapses or associational/commisural (A/C) synapses results in the activation of these presynaptic ionotropic KARs. These results, along with previous studies, indicate that KARs, through the endogenous release of glutamate, mediate excitatory postsynaptic potentials (EPSPs), alter presynaptic excitability, and modulate transmitter release.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cells, Cultured
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / physiology
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GABA Antagonists / pharmacology
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Glutamic Acid / metabolism
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Hippocampus / cytology
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Hippocampus / metabolism*
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In Vitro Techniques
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Kainic Acid / metabolism
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Kainic Acid / pharmacology
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Mossy Fibers, Hippocampal / metabolism*
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N-Methylaspartate / metabolism
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N-Methylaspartate / pharmacology
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Patch-Clamp Techniques
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Potassium / pharmacology
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Presynaptic Terminals / metabolism*
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Rats
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Rats, Sprague-Dawley
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Receptors, AMPA / antagonists & inhibitors
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Receptors, Kainic Acid / agonists
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Receptors, Kainic Acid / metabolism*
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Synapses / metabolism*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
Substances
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Excitatory Amino Acid Antagonists
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GABA Antagonists
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Receptors, AMPA
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Receptors, Kainic Acid
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Glutamic Acid
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N-Methylaspartate
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Potassium
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Kainic Acid