Crus cerebri lesions abolish amphetamine-induced ascorbate release in the rat neostriatum

An increase in the concentration of ascorbate in the extracellular fluid of the rat striatum following systemic amphetamine administration previously has been demonstrated with the use of in vivo electrochemistry, push-pull cannula and in vivo dialysis. In this report, the effect of infusions of amphetamine into the substantia nigra on extracellular ascorbate levels in the striatum is further investigated by in vivo electrochemistry. Electrolytic lesions in the crus cerebri of the striatonigral pathway abolish this effect. Furthermore, these lesions abolish the effect of systemic amphetamine in the striatum ipsilateral to the lesion but not on the contralateral side. This phenomenon is independent of neostriatal dopamine or gamma-aminobutyric acid since levels were shown to be unchanged relative to the intact side. These results lend further support to the hypothesis that ascorbate secretion in the striatum after amphetamine is mediated in the central nervous system, and indicate that a pathway that courses through the crus cerebri is necessary for this release.