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dc.contributor.authorBird, MK
dc.contributor.authorReid, CA
dc.contributor.authorChen, F
dc.contributor.authorTan, HO
dc.contributor.authorPetrou, S
dc.contributor.authorLawrence, AJ
dc.date.accessioned2014-05-22T07:37:12Z
dc.date.available2014-05-22T07:37:12Z
dc.date.issued2010-03-01
dc.identifierpii: S1461145709990162
dc.identifier.citationBird, M. K., Reid, C. A., Chen, F., Tan, H. O., Petrou, S. & Lawrence, A. J. (2010). Cocaine-mediated synaptic potentiation is absent in VTA neurons from mGlu5-deficient mice. INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY, 13 (2), pp.133-141. https://doi.org/10.1017/S1461145709990162.
dc.identifier.issn1461-1457
dc.identifier.urihttp://hdl.handle.net/11343/32969
dc.description© 2009 CINP. Online edition of the journal is available at http://journals.cambridge.org/action/displayJournal?jid=PNP
dc.description.abstractDrugs of abuse have the ability to instantiate plastic adaptations within the central nervous system, and this property may relate to the development and persistence of addiction. In this context, a single exposure to cocaine in rodents may induce synaptic plasticity by increasing the AMPA/NMDA receptor excitatory post-synaptic current (EPSC) amplitude ratio in dopaminergic cells of the ventral tegmental area (VTA). Here, we examine the role of the metabotropic glutamate 5 (mGlu5) receptor in this regard using a genetic mouse model. The control AMPA/NMDA EPSC ratio is reduced in mGlu5-deficient mice compared to wild-types. Moreover, cocaine-induced enhancement of this EPSC ratio is also absent in mutant mice, which suggests that mGlu5 receptors are required for single-dose cocaine-induced plasticity onto VTA cells. While the temporal profile of hyperactivity to acute cocaine is altered in mGlu5-deficient mice; these mice still develop and express sensitized psychomotor responses to cocaine. These data suggest that the mGlu5 receptor is required for cocaine-induced plasticity in VTA dopaminergic cells. In contrast, the mGlu5 receptor may not be essential for psychostimulant behavioural sensitization; although it probably impacts other aspects drug addiction, such as motivation to self-administer.
dc.languageEnglish
dc.publisherOXFORD UNIV PRESS
dc.subjectcocaine
dc.subjectmGlu5 receptor
dc.subjectsensitization
dc.subjectsynaptic plasticity
dc.subjectVTA
dc.titleCocaine-mediated synaptic potentiation is absent in VTA neurons from mGlu5-deficient mice
dc.typeJournal Article
dc.identifier.doi10.1017/S1461145709990162
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliationHoward Florey Institute
melbourne.affiliation.departmentCentre for Neuroscience
melbourne.affiliation.departmentDepartment of Medicine, Austin Campus
melbourne.publication.statusPublished
melbourne.source.titleInternational Journal of Neuropsychopharmacology
melbourne.source.volume13
melbourne.source.issue2
melbourne.source.pages133-141
melbourne.elementsid327716
melbourne.contributor.authorBIRD, MICHAEL
melbourne.contributor.authorReid, Christopher
melbourne.contributor.authorPetrou, Steven
melbourne.contributor.authorLawrence, Andrew
dc.identifier.eissn1469-5111
melbourne.accessrightsOpen Access


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