Possible role of glutamatergic neurotransmission in regulating ethanol-evoked brain ascorbate release

It was found that systemic application of ethanol induced brain ascorbate (AA) release. In order to study the mechanism of ethanol-evoked AA release, the role of brain glutamatergic neurotransmission was investigated using in vivo voltammetry in the striatum of freely moving rats. Pretreatment with L-trans-pyrrolidine-2,4-dicarboxylate (PDC, 10 nmol, i.c.v.), a glutamate (Glu) uptake blocker, potentiated ethanol (1 g/kg, intraperitoneal injection, i.p.)-evoked release of brain AA. N-methyl-D-aspartate (NMDA, 1 nmol, i.c.v.) produced a fast transient increase in extracellular AA, whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA, 1 nmol, i.c.v.) produced a decrease in extracellular AA (75.8 +/- 3% of control). Kainate (KA, 1 nmol, i.c.v.) produced an initial decrease (48.7 +/- 11.7% of control) then an increase (250 +/- 68.5% of control) in extracellular AA. These results suggest that systemic administration of ethanol may affect the release or uptake of brain glutamatergic neurotransmitters which appear to regulate brain AA release. The NMDA, but not the non-NMDA, type of Glu receptor may be responsible for this regulation.