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dc.contributor.authorHascup, Kevin N.
dc.contributor.authorBao, Xiaodong
dc.contributor.authorHascup, Erin R.
dc.contributor.authorHui, Dongwei
dc.contributor.authorXu, Wenhao
dc.contributor.authorPomerleau, Francois
dc.contributor.authorHuettl, Peter
dc.contributor.authorMichaelis, Mary Lou
dc.contributor.authorMichaelis, Elias K.
dc.contributor.authorGerhardt, Greg A.
dc.date.accessioned2014-04-17T18:34:19Z
dc.date.available2014-04-17T18:34:19Z
dc.date.issued2011-03-29
dc.identifier.citationHascup, Kevin N, Xiaodong Bao, Erin R Hascup, Dongwei Hui, Wenhao Xu, Francois Pomerleau, Peter Huettl, Mary L Michaelis, Elias K Michaelis, and Greg A Gerhardt. 2011. “Differential Levels of Glutamate Dehydrogenase 1 (GLUD1) in Balb/c and C57BL/6 Mice and the Effects of Overexpression of the Glud1 Gene on Glutamate Release in Striatum.” ASN NEURO 3 (2). http://dx.doi.org/10.1042/AN20110005. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086280
dc.identifier.urihttp://hdl.handle.net/1808/13536
dc.description.abstractWe have previously shown that overexpression of the Glud1 (glutamate dehydrogenase 1) gene in neurons of C57BL/6 mice results in increased depolarization-induced glutamate release that eventually leads to selective neuronal injury and cell loss by 12 months of age. However, it is known that isogenic lines of Tg (transgenic) mice produced through back-crossing with one strain may differ in their phenotypic characteristics from those produced using another inbred mouse strain. Therefore, we decided to introduce the Glud1 transgene into the Balb/c strain that has endogenously lower levels of GLUD1 (glutamate dehydrogenase 1) enzyme activity in the brain as compared with C57BL/6. Using an enzyme-based MEA (microelectrode array) that is selective for measuring glutamate in vivo, we measured depolarization-induced glutamate release. Within a discrete layer of the striatum, glutamate release was significantly increased in Balb/c Tg mice compared with wt (wild-type) littermates. Furthermore, Balb/c mice released approx. 50–60% of the amount of glutamate compared with C57BL/6 mice. This is similar to the lower levels of endogenous GLUD1 protein in Balb/c compared with C57BL/6 mice. The development of these Glud1-overexpressing mice may allow for the exploration of key molecular events produced by chronic exposure of neurons to moderate, transient increases in glutamate release, a process hypothesized to occur in neurodegenerative disorders.
dc.description.sponsorshipThis work was supported by the NSF (National Science Foundation) [grant number EEC-0310723]; NIH/NIDA (National Institutes of Health/National Institute on Drug Abuse) [grant number DA017186]; CEBRA, Phase II, NIA, [grant number AG12993]; NIAAA (National Institute of Alcohol Abuse and Alcoholism) [grant numbers AA11419, AA04732, AA12276]; NSF [grant numbers DBI-9987807, DBI-0352848]; NIDA [grant number DA017186]; NINDS (National Institute of Neurological Disorders and Strokes) [grant number NS39787]; NIMH (National Institute of Mental Health) [grant number MH58414]; NIDA Training [grant number DA022738]; NIDA [grant number DA015088], The Kansas Technology Enterprise Corporation, The Miller, Hedwig and Wilbur Fund, and The University of Kansas Research Development Fund.
dc.publisherPortland Press Limited
dc.rightsThe Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/2.5/
dc.subjectAmperometry
dc.subjectBiosensor
dc.subjectElectrochemistry
dc.subjectExcitotoxicity
dc.subjectNeurodegeneration
dc.subjectNeurotransmission
dc.titleDifferential levels of glutamate dehydrogenase 1 (GLUD1) in Balb/c and C57BL/6 mice and the effects of overexpression of the Glud1 gene on glutamate release in striatum
dc.typeArticle
kusw.kuauthorBao, Xiaodong
kusw.kuauthorHui, Dongwei
kusw.kuauthorMichaelis, Mary L.
kusw.kuauthorMichaelis, Elias K.
kusw.kudepartmentDepartment of Pharmacology and Toxicology
kusw.oastatusfullparticipation
dc.identifier.doi10.1042/AN20110005
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item meets KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


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The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as: The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.