Abstract
We report that kainate receptors are present on presynaptic GABAergic terminals contacting interneurons and that their activation increases GABA release. Application of kainate increased the frequency of miniature inhibitory postsynaptic currents recorded in CA1 interneurons. Local applications of glutamate but not of AMPA or NMDA also increased GABA quantal release. Application of kainate as well as synaptically released glutamate reduced the number of failures of GABAergic neurotransmission between interneurons. Thus, activation of presynaptic kainate receptors increases the probability of GABA release at interneuron-interneuron synapses. Glutamate may selectively control the communication between interneurons by increasing their mutual inhibition.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Excitatory Amino Acid Agonists / pharmacology
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Glutamic Acid / pharmacology
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Hippocampus / drug effects
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Hippocampus / physiology
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Interneurons / drug effects
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Interneurons / physiology*
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Kainic Acid / pharmacology
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiology*
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Rats
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Rats, Wistar
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Receptors, Kainic Acid / drug effects
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Receptors, Kainic Acid / physiology*
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Receptors, Presynaptic / drug effects
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Receptors, Presynaptic / physiology*
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Signal Transduction / drug effects
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Signal Transduction / physiology
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gamma-Aminobutyric Acid / metabolism*
Substances
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Excitatory Amino Acid Agonists
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Receptors, Kainic Acid
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Receptors, Presynaptic
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Glutamic Acid
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gamma-Aminobutyric Acid
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Kainic Acid