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Glutamate is the predominant excitatory neurotransmitter in the brain, and excess activation of glutamate receptors can cause neuronal dysfunction and death. Glutamate transporters regulate the extracellular concentration of glutamate.\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101 is the most abundant glutamate transporter, and accounts for most of the glutamate transport in the brain. Administration of ceftriaxone, an antibiotic that increases the functional expression of\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101, can improve the behavioral phenotype of the R6\/2 mouse model of\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    . To test the hypothesis that\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101 expression critically affects the\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    disease process, we generated a novel mouse model that is heterozygous for the null allele of\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101 and carries the R6\/2 transgene (double mutation). We demonstrated that the protein expression of total\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101, as well as two of its isoforms, is decreased within the cortex and striatum of 12\u2010week\u2010old R6\/2 mice, and that the expression of\n                    <jats:styled-content style=\"fixed-case\">EAAC<\/jats:styled-content>\n                    1 was decreased in the striatum. Protein expression of\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101 was further decreased in the cortex and striatum of the double mutation mice compared with the R6\/2 mice at 11\u00a0weeks. However, the effects of the R6\/2 transgene on weight loss, accelerating rotarod, climbing and paw\u2010clasping were not exacerbated in these double mutants. Na\n                    <jats:sup>+<\/jats:sup>\n                    \u2010dependent glutamate uptake into synapatosomes isolated from the striatum and cortex of 11\u2010week\u2010old R6\/2 mice was unchanged compared with controls. These results suggest that changes in\n                    <jats:styled-content style=\"fixed-case\">GLT<\/jats:styled-content>\n                    \u20101 expression or function\n                    <jats:italic>per se<\/jats:italic>\n                    are unlikely to potentiate or ameliorate the progression of\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/ejn.12202","type":"journal-article","created":{"date-parts":[[2013,4,16]],"date-time":"2013-04-16T02:36:40Z","timestamp":1366079800000},"page":"2477-2490","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Decreased expression of\n                    <scp>GLT<\/scp>\n                    \u20101 in the R6\/2 model of Huntington's disease does not worsen disease progression"],"prefix":"10.1111","volume":"38","author":[{"given":"Geraldine T.","family":"Petr","sequence":"first","affiliation":[{"name":"Department of Neurology and the F.M. 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Kirby Neurobiology Center Children's Hospital Boston Boston MA USA"},{"name":"Program in Neuroscience Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet M.","family":"Dubinsky","sequence":"additional","affiliation":[{"name":"Department of Neuroscience University of Minnesota Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiye","family":"Aoki","sequence":"additional","affiliation":[{"name":"Center for Neural Science New York University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Rosenberg","sequence":"additional","affiliation":[{"name":"Department of Neurology and the F.M. 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