The possible influence of the corticostriatal (glutamatergic) pathway on denervation-induced striatal dopamine target cell supersensitivity has been investigated in the rat by measuring the changes in striatal acetylcholine levels induced by the dopamine agonist pergolide and the basal dopamine D2-receptor density after combined 6-hydroxydopamine-induced lesion of the substantia nigra and cortical ablation. Lesion of the nigrostriatal dopaminergic pathway alone enhanced the ability of pergolide (0.06-1 mg/kg i.p.) to increase acetylcholine levels and increased the maximal density of [3H]spiperone binding sites in the striatum. Similar changes in these biochemical parameters were observed after combined cortical ablation and nigral lesion. Cortical ablation by itself slightly diminished acetylcholine levels and reduced by 30% [3H]spiperone binding site density in the striatum. These results indicate that the corticostriatal tract does not influence striatal dopamine target cell supersensitivity caused by dopaminergic denervation.
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