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dc.contributor.authorMichaelis, Elias K.
dc.contributor.authorWang, Xinkun
dc.contributor.authorPal, Ranu
dc.contributor.authorBao, Xiaodong
dc.contributor.authorHascup, Kevin N.
dc.contributor.authorWang, Yongfu
dc.contributor.authorWang, Wen-Tung
dc.contributor.authorHui, Dongwei
dc.contributor.authorAgbas, Abdulbaki
dc.contributor.authorChoi, In-Young
dc.contributor.authorBelousov, Andrei B.
dc.contributor.authorGerhardt, Greg A.
dc.date.accessioned2017-06-27T17:26:33Z
dc.date.available2017-06-27T17:26:33Z
dc.date.issued2011-09
dc.identifier.citationMichaelis, E. K., Wang, X., Pal, R., Bao, X., Hascup, K. N., Wang, Y., … Gerhardt, G. A. (2011). Neuronal Glud1 (Glutamate Dehydrogenase 1) Over-Expressing Mice: Increased Glutamate Formation and Synaptic Release, Loss of Synaptic Activity, and Adaptive Changes in Genomic Expression. Neurochemistry International, 59(4), 473–481. http://doi.org/10.1016/j.neuint.2011.03.003en_US
dc.identifier.urihttp://hdl.handle.net/1808/24649
dc.description.abstractGlutamate dehydrogenase 1 (GLUD1) is a mitochondrial enzyme expressed in all tissues, including brain. Although this enzyme is expressed in glutamatergic pathways, its function as a regulator of glutamate neurotransmitter levels is still not well defined. In order to gain an understanding of the role of GLUD1 in the control of glutamate levels and synaptic release in mammalian brain, we generated transgenic (Tg) mice that over-express this enzyme in neurons of the central nervous system. The Tg mice have increased activity of GLUD, as well as elevated levels and increased synaptic and depolarization-induced release of glutamate. These mice suffer age-associated losses of dendritic spines, nerve terminals, and neurons. The neuronal losses and dendrite structural changes occur in select regions of the brain. At the transcriptional level in the hippocampus, cells respond by increasing the expression of genes related to neurite growth and synapse formation, indications of adaptive or compensatory responses to the effects of increases in the release and action of glutamate at synapses. Because these Tg mice live to a relatively old age they are a good model of the effects of a “hyperglutamatergic” state on the aging process in the nervous system. The mice are also useful in defining the molecular pathways affected by the over-activation of GLUD in glutamatergic neurons of the brain and spinal cord.en_US
dc.publisherElsevieren_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.subjectGlutamate dehydrogenaseen_US
dc.subjectDepolarization-induced glutamate releaseen_US
dc.subjectSpine lossen_US
dc.subjectSynapse lossen_US
dc.subjectLTPen_US
dc.subjectAgingen_US
dc.subjectTranscriptomic changesen_US
dc.titleNeuronal Glud1 (Glutamate Dehydrogenase 1) Over-Expressing Mice: Increased Glutamate Formation and Synaptic Release, Loss of Synaptic Activity, and Adaptive Changes in Genomic Expressionen_US
dc.typeArticleen_US
kusw.kuauthorMichaelis, Elias K.
kusw.kuauthorWang, Xinkun
kusw.kuauthorPal, Ranu
kusw.kuauthorHui, Dongwei
kusw.kuauthorAgbas, Abdulbaki
kusw.kudepartmentHiguchi Biosciences Centeren_US
kusw.oanotesPer SHERPA/RoMEO 6/27/2017: Author's Pre-print: green tick author can archive pre-print (ie pre-refereeing) Author's Post-print: green tick author can archive post-print (ie final draft post-refereeing) Publisher's Version/PDF: cross author cannot archive publisher's version/PDF General Conditions:

Authors pre-print on any website, including arXiv and RePEC Author's post-print on author's personal website immediately Author's post-print on open access repository after an embargo period of between 12 months and 48 months Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months Author's post-print may be used to update arXiv and RepEC Publisher's version/PDF cannot be used Must link to publisher version with DOI Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
en_US
dc.identifier.doi10.1016/j.neuint.2011.03.003en_US
dc.identifier.orcidhttps://orcid.org/0000-0003-1377-0509 https://orcid.org/0000-0003-3499-0586
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC3152645en_US
dc.rights.accessrightsopenAccess


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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.