title: Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area.
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.
authors.affiliation: Department of Basic Neurosciences, Medical Faculty, University of Geneva, Geneva, Switzerland.
authors.forename: Manuel
authors.initials: M
authors.lastname: Mameli
authors.forename: Camilla
authors.initials: C
authors.lastname: Bellone
authors.forename: Matthew T C
authors.initials: MT
authors.lastname: Brown
authors.forename: Christian
authors.initials: C
authors.lastname: Lüscher
mesh_terms: D000818:Animals; D003042:Cocaine / Q000494:pharmacology*; D019970:Cocaine-Related Disorders / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology*; D004195:Disease Models, Animal; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology*; D051379:Mice; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D009924:Organ Culture Techniques; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology; D017557:Ventral Tegmental Area / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D018765:Dopamine Uptake Inhibitors; D018698:Glutamic Acid; D003042:Cocaine