Abstract
Exposure to cocaine, and likely other drugs of abuse, generates α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-silent glutamatergic synapses in the nucleus accumbens. These immature synaptic contacts evolve after drug withdrawal to redefine the neurocircuital properties. These results raise at least three critical questions: (1) what are the molecular and cellular mechanisms that mediate drug-induced generation of silent synapses; (2) how are neurocircuits remodeled upon generation and evolution of drug-generated silent synapses; and (3) what behavioral consequences are produced by silent synapse-based circuitry remodeling? This short review analyzes related experimental results, and extends them to some speculations.
Keywords:
accumbens; anti-addictive; circuitry remodeling; cocaine; incubation; silent synapse.
© The Author 2015. Published by Oxford University Press on behalf of CINP.
Publication types
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Review
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Research Support, N.I.H., Extramural
MeSH terms
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Adaptation, Physiological
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Adaptation, Psychological
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Animals
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Behavior, Addictive / metabolism
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Behavior, Addictive / physiopathology
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Behavior, Addictive / psychology
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Central Nervous System Stimulants / adverse effects*
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Cocaine / adverse effects*
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Cocaine-Related Disorders / metabolism
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Cocaine-Related Disorders / physiopathology*
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Cocaine-Related Disorders / psychology
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Drug Users / psychology*
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Excitatory Postsynaptic Potentials
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Glutamic Acid / metabolism
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Humans
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Neuronal Plasticity / drug effects*
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Nucleus Accumbens / drug effects*
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Nucleus Accumbens / metabolism
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Nucleus Accumbens / physiopathology
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Receptors, Glutamate / drug effects*
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Receptors, Glutamate / metabolism
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / metabolism
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Synaptic Transmission / drug effects*
Substances
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Central Nervous System Stimulants
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Receptors, Glutamate
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Receptors, N-Methyl-D-Aspartate
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alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, human
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Glutamic Acid
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Cocaine