Abstract
Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Amygdala / physiology*
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Animals
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Calcium / physiology
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Egtazic Acid / analogs & derivatives
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Egtazic Acid / pharmacology
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Electric Stimulation
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Excitatory Amino Acid Antagonists / pharmacology
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GluK2 Kainate Receptor
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In Vitro Techniques
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Isoxazoles / pharmacology
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Male
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Neurons / physiology*
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Propionates / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, Kainic Acid / drug effects
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Receptors, Kainic Acid / genetics
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Receptors, Kainic Acid / physiology*
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Reverse Transcriptase Polymerase Chain Reaction
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Synapses / physiology*
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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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Gluk1 kainate receptor
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Isoxazoles
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Propionates
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Receptors, Kainic Acid
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1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
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alpha-amino-3-hydroxy-5-tert-butyl-4-isoxazolepropionate
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Egtazic Acid
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Calcium