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Neurochem.<\/jats:italic> (2012) <jats:bold>121<\/jats:bold>, 629\u2013638.<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>A corticostriatal\u2010dependent deficit in the release of ascorbate (AA), an antioxidant vitamin and neuromodulator, occurs concurrently in striatum with dysfunctional GLT1\u2010dependent uptake of glutamate in the R6\/2 mouse model of Huntington\u2019s disease (HD), an autosomal dominant condition characterized by overt corticostriatal dysfunction. To determine if deficient striatal AA release into extracellular fluid is related to altered GLT1 activity in HD, symptomatic R6\/2 mice between 6 and 9\u2003weeks of age and age\u2010matched wild\u2010type (WT) mice received single daily injections of 200\u2003mg\/kg ceftriaxone, a \u03b2\u2010lactam antibiotic that elevates the functional expression of GLT1, or saline vehicle for five consecutive days. On the following day, <jats:italic>in vivo<\/jats:italic> voltammetry was coupled with corticostriatal afferent stimulation to monitor evoked release of AA into striatum. In saline\u2010treated mice, we found a marked decrease in evoked extracellular AA in striatum of R6\/2 relative to WT. Ceftriaxone, in contrast, restored striatal AA in R6\/2 mice to WT levels. In addition, intra\u2010striatal infusion of either the GLT1 inhibitor dihydrokainic acid or <jats:sc>dl<\/jats:sc>\u2010threo\u2010beta\u2010benzyloxyaspartate blocked evoked striatal AA release. Collectively, our results provide compelling evidence for a link between GLT1 activation and release of AA into the striatal extracellular fluid, and suggest that dysfunction of this system is a key component of HD pathophysiology.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1471-4159.2012.07691.x","type":"journal-article","created":{"date-parts":[[2012,2,14]],"date-time":"2012-02-14T15:45:22Z","timestamp":1329234322000},"page":"629-638","source":"Crossref","is-referenced-by-count":44,"title":["Up\u2010regulation of GLT1 reverses the deficit in cortically evoked striatal ascorbate efflux in the R6\/2 mouse model of Huntington\u2019s disease"],"prefix":"10.1111","volume":"121","author":[{"given":"Benjamin R.","family":"Miller","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenelle L.","family":"Dorner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kendra 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