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.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Mameli M,Bellone C,Brown MT,Lüscher C

doi

10.1038/nn.2763

subject

Has Abstract

pub_date

2011-04-01 00:00:00

pages

414-6

issue

4

eissn

1097-6256

issn

1546-1726

pii

nn.2763

journal_volume

14

pub_type

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