It is common knowledge that the main mediators in the pathogenesis of Parkinson's disease are oxidative stress, excitotoxicity and mitochondrial dysfunction. Increased glutamate concentrations can be linked, directly or indirectly, to all of these processes. Extracellular glutamate concentrations are determined by an interplay between vesicular glutamate transporters (VGLUTs), glial high-affinity Na+/K+-dependent glutamate transporters (GLAST and GLT-1) and the cystine/glutamate antiporter. Using semi-quantitative Western blotting, we studied the expression levels of VGLUT1, GLAST, GLT-1 and xCT, the specific subunit of the cystine/glutamate antiporter, in the striatum of rats at different survival times (3, 5 and 12 weeks) after unilateral 6-OHDA injection into the medial forebrain bundle. Given earlier observations by Meshul et al. (1999) of a biphasic change in extracellular glutamate levels after 6-OHDA lesioning, with increases 1 month post-lesion and decreases 3 months post-lesion, our data are suggestive of an important role of the cystine/glutamate antiporter and VGLUT1 in determining the aberrant extracellular glutamate levels in the 6-OHDA rat model. Modulation of one or more of these transporters might help to normalize the extracellular glutamate levels and prevent further excitotoxic and oxidative damage.
Original languageEnglish
Title of host publicationWierzba IV, Poland
Publication statusPublished - 2008

    Research areas

  • Parkinson's disease, glutamate transport, striatum

ID: 1749003