Involvement of the corticostriatal glutamatergic pathway in ethanol‐induced ascorbic acid release in rat striatum

Abstract

The mechanism of ethanol-induced ascorbic acid (AA) release in striatum is not well understood. In the present work, the possible involvement of NMDA receptors in the corticostriatal pathway was studied by microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg i.p.) stimulated significant striatal AA release to more than 200% above the baseline. This effect of ethanol could be partially antagonized by amantadine, a non-selective NMDA receptor antagonist and dopamine releaser, at a dose of 200 mg/kg i.p. and significantly antagonized by MK-801, a non-competitive NMDA receptor antagonist, at the doses of 0.5 and 1.0 mg/kg i.p. Furthermore, deafferentation of the glutamatergic projection from cortex to striatum by undercutting the prefrontal cortex completely eliminated ethanol-induced AA release in rat striatum. The basal level of AA in striatum could only be reduced by high doses of MK-801, but not by low doses of MK-801, amantadine or decortication. The results further confirm that NMDA receptors are involved in ethanol-induced AA release and provide the first evidence for the necessity of the activation of corticostriatal glutamatergic pathway in ethanol-induced AA release in rat striatum.