Glutamate Receptors on Dopamine Neurons Control the Persistence of Cocaine Seeking
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Show full item recordcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/8033
comunitat-uji-handle3:10234/8636
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http://dx.doi.org/10.1016/j.neuron.2008.07.010 |
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Title
Glutamate Receptors on Dopamine Neurons Control the Persistence of Cocaine SeekingAuthor (s)
Date
2008-08Publisher
ElsevierISSN
0896-6273Bibliographic citation
Neuron, 59, 3, p. 497–508Type
info:eu-repo/semantics/articlePublisher version
http://www.sciencedirect.com/science/article/pii/S0896627308005825Version
info:eu-repo/semantics/publishedVersionSubject
Abstract
Cocaine strengthens excitatory synapses onto midbrain dopamine neurons through the synaptic delivery of GluR1-containing AMPA receptors. This cocaine-evoked plasticity depends on NMDA receptor activation, but its ... [+]
Cocaine strengthens excitatory synapses onto midbrain dopamine neurons through the synaptic delivery of GluR1-containing AMPA receptors. This cocaine-evoked plasticity depends on NMDA receptor activation, but its behavioral significance in the context of addiction remains elusive. Here, we generated mice lacking the GluR1, GluR2, or NR1 receptor subunits selectively in dopamine neurons. We report that in midbrain slices of cocaine-treated mice, synaptic transmission was no longer strengthened when GluR1 or NR1 was abolished, while in the respective mice the drug still induced normal conditioned place preference and locomotor sensitization. In contrast, extinction of drug-seeking behavior was absent in mice lacking GluR1, while in the NR1 mutant mice reinstatement was abolished. In conclusion, cocaine-evoked synaptic plasticity does not mediate concurrent short-term behavioral effects of the drug but may initiate adaptive changes eventually leading to the persistence of drug-seeking behavior. [-]
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Copyright © 2008 Elsevier Inc. All rights reserved
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