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dc.contributor.authorPendyam, Sandeepeng
dc.contributor.authorMohan, Ashwin, 1978-eng
dc.contributor.authorKalivas, Peter W., 1952-eng
dc.contributor.authorNair, Satish S., 1960-eng
dc.date.issued2009-02eng
dc.descriptionNotice: this is the author's version of a work that was accepted for publication in Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neuroscience, Vol. 158, Issue #4 (2008) doi:10.1016/j.neuroscience.2008.11.014 . http://journals.elsevier.com/03064522/neuroscience/eng
dc.description.abstractChronic cocaine administration causes instability in extracellular glutamate in the nucleus accumbens that is thought to contribute to the vulnerability to relapse. A computational framework was developed to model glutamate in the extracellular space, including synaptic and nonsynaptic glutamate release, glutamate elimination by glutamate transporters and diffusion, and negative feedback on synaptic release via metabotropic glutamate receptors (mGluR2/3). This framework was used to optimize the geometry of the glial sheath surrounding excitatory synapses, and by inserting physiological values, accounted for known stable extracellular, extrasynaptic concentrations of glutamate measured by microdialysis and glutamatergic tone on mGluR2/3. By using experimental values for cocaine-induced reductions in cystine-glutamate exchange and mGluR2/3 signaling, the computational model successfully represented the experimentally observed increase in glutamate that is seen in rats during cocaine-seeking. This model provides a mathematical framework for describing how pharmacological or pathological conditions influence glutamate transmission measured by microdialysis.eng
dc.identifier.citationPendyam S, Mohan A, Kalivas PW, Nair SS (2009) Computational model of extracellular glutamate in the nucleus accumbens incorporates neuroadaptations by chronic cocaine, Neuroscience 158(4):1266-76.eng
dc.identifier.urihttp://hdl.handle.net/10355/9787eng
dc.languageEnglisheng
dc.publisherElseviereng
dc.relation.ispartofcollectionBiological Engineering publications (MU)eng
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. College of Engineering. Department of Biological Engineeringeng
dc.rightsOpenAccess.eng
dc.rights.licenseThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.eng
dc.subjectcocaine addictioneng
dc.subjectglutamate transmissioneng
dc.subject.lcshCocaine abuseeng
dc.subject.lcshGlutamic acideng
dc.subject.lcshNucleus accumbenseng
dc.titleComputational model of extracellular glutamate in the nucleus accumbens predicts neuroadaptations by chronic cocaineeng
dc.typeArticleeng


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