Differential effects of corticostriatal and thalamostriatal deafferentation on expression of the glutamate transporter GLT1 in the rat striatum

This study compared the effects of the disruption of the two main presumabl y glutamatergic striatal inputs, the corticostriatal and thalamostriatal pa thways, on GLT1 expression in the rat striatum, using in situ hybridization and immunohistochemistry. Unilateral ibotenate-induced thalamic lesion pro duced no significant changes in striatal GLT1 mRNA labeling and immunostain ing as assessed at 5 and 12 days postlesion. In contrast, significant incre ases in both parameters were measured after bilateral cortical lesion by su perficial thermocoagulation, GLT1 mRNA levels increased predominantly in th e dorsolateral part of the striatum; there, the increases were significant at 5 (+84%), 12 (+101%), and 21 (+45%) but not at 35 days postlesion. GLT1 immunostaining increased significantly and homogeneously by 17-26% at 12 an d 21 days postlesion, The increase in GLT1 expression at 12 days postlesion was further confirmed by western blot analysis; in contrast, a 36% decreas e in glutamate uptake activity was measured at the same time point. These d ata indicate that striatal GLT1 expression depends on corticostriatal but n ot thalamostriatal innervation. Comparison of our results with previous dat a showing that cortical lesion by aspiration downregulates striatal GLT1 ex pression further suggests that differential changes in GLT1 expression, and thus presumably in glial cell function, may occur in the target striatum d epending on the way the cortical neurons degenerate.