Abstract
Synaptic inhibition is a vital component in the control of cell excitability within the brain. Here we report a newly identified form of inhibitory synaptic plasticity, termed depolarization-induced potentiation of inhibition, in rodents. This mechanism strongly potentiated synaptic transmission from interneurons to Purkinje cells after the termination of depolarization-induced suppression of inhibition. It was triggered by an elevation of Ca(2+) in Purkinje cells and the subsequent retrograde activation of presynaptic NMDA receptors. These glutamate receptors promoted the spontaneous release of Ca(2+) from presynaptic ryanodine-sensitive Ca(2+) stores. Thus, NMDA receptor-mediated facilitation of transmission at this synapse provides a regulatory mechanism that can dynamically alter the synaptic efficacy at inhibitory synapses.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Cadmium / pharmacology
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Calcium / metabolism
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Cerebellum / cytology*
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Chelating Agents / pharmacology
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Dose-Response Relationship, Drug
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Drug Interactions
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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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Evoked Potentials / drug effects
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Evoked Potentials / radiation effects
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Excitatory Amino Acid Antagonists / pharmacology
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Glutamate Decarboxylase / metabolism
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Immunohistochemistry / methods
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In Vitro Techniques
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Interneurons / metabolism*
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Isoenzymes / metabolism
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Membrane Potentials / drug effects
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Membrane Potentials / radiation effects
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N-Methylaspartate / pharmacology
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Neural Inhibition / physiology
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology
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Neuronal Plasticity / radiation effects
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Patch-Clamp Techniques / methods
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Piperidines / pharmacology
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Presynaptic Terminals / metabolism
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Purkinje Cells / metabolism*
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Pyrazoles / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Rimonabant
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Ryanodine / pharmacology
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Sodium Channel Blockers / pharmacology
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Synapses / metabolism*
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Synaptic Transmission / physiology
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Synaptophysin / metabolism
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Tetrodotoxin / pharmacology
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Time Factors
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gamma-Aminobutyric Acid / metabolism*
Substances
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Chelating Agents
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Excitatory Amino Acid Antagonists
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Isoenzymes
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NR1 NMDA receptor
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NR2A NMDA receptor
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Piperidines
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Pyrazoles
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Receptors, N-Methyl-D-Aspartate
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Sodium Channel Blockers
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Synaptophysin
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Cadmium
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Ryanodine
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Tetrodotoxin
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Egtazic Acid
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gamma-Aminobutyric Acid
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N-Methylaspartate
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Glutamate Decarboxylase
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glutamate decarboxylase 1
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glutamate decarboxylase 2
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
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Rimonabant
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Calcium