Abstract
The manner in which drug-evoked synaptic plasticity affects reward circuits remains largely elusive. We found that cocaine reduced NMDA receptor excitatory postsynaptic currents and inserted GluA2-lacking AMPA receptors in dopamine neurons of mice. Consequently, a stimulation protocol pairing glutamate release with hyperpolarizing current injections further strengthened synapses after cocaine treatment. Our data suggest that early cocaine-evoked plasticity in the ventral tegmental area inverts the rules for activity-dependent plasticity, eventually leading to addictive behavior.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cocaine / pharmacology*
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Cocaine-Related Disorders / genetics
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Cocaine-Related Disorders / metabolism*
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Cocaine-Related Disorders / physiopathology*
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Disease Models, Animal
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Dopamine Uptake Inhibitors / pharmacology
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Glutamic Acid / physiology*
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Mice
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Neuronal Plasticity / drug effects*
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Neuronal Plasticity / physiology
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Organ Culture Techniques
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Synaptic Transmission / drug effects*
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Synaptic Transmission / physiology
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Ventral Tegmental Area / drug effects*
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Ventral Tegmental Area / metabolism
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Ventral Tegmental Area / physiopathology*
Substances
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Dopamine Uptake Inhibitors
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Glutamic Acid
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Cocaine