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Title

Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area

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Published in Nature Neuroscience. 2011, vol. 14, no. 4, p. 414-6
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.
Keywords AnimalsCocaine/pharmacologyCocaine-Related Disorders/genetics/metabolism/physiopathologyDisease Models, AnimalDopamine Uptake Inhibitors/pharmacologyGlutamic Acid/physiologyMiceNeuronal Plasticity/drug effects/physiologyOrgan Culture TechniquesSynaptic Transmission/drug effects/physiologyVentral Tegmental Area/drug effects/metabolism/physiopathology
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PMID: 21336270
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Article (Published version) (485 Kb) - document accessible for UNIGE members only Limited access to UNIGE
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Research group Mécanismes cellulaires de la dépendance et de l'addiction (520)
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MAMELI, Manuel et al. Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area. In: Nature Neuroscience, 2011, vol. 14, n° 4, p. 414-6. https://archive-ouverte.unige.ch/unige:26927

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Deposited on : 2013-03-25

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