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Article

Up-regulation of GLT1 reverses the deficit in cortically evoked striatal ascorbate efflux in the R6/2 mouse model of Huntington's disease.

Journal of neurochemistry - 1 May 2012

Miller Benjamin R, Dorner Jenelle L, Bunner Kendra D, Gaither Thomas W, Klein Emma L, Barton Scott J, Rebec George V

Abstract excerpt

A corticostriatal-dependent deficit in the release of ascorbate (AA), an antioxidant vitamin and neuromodulator, occurs concurrently in striatum with dysfunctional GLT1-dependent uptake of glutamate in the R6/2 mouse model of Huntington's disease (HD), an autosomal dominant condition characterized by overt corticostriatal dysfunction. To determine if deficient striatal AA release into extracellular fluid is...

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Identifiers

PMID: 22332910
DOI: 10.1111/j.1471-4159.2012.07691.x
PMCID: PMC3325322

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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