Cortical ablation and drug-induced changes in striatal ascorbic acid oxidation and behavior in the rat

Rats whose frontoparietal cortex had been bilaterally ablated were allowed 21 days for recovery and then treated with apomorphine (APO), 1 mg/kg SC or scopolamine (SCOP), 0.6 mg/kg SC. Soon after a behavioral test, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), and dehydroascorbic acid (DHAA) levels were determined by HPLC/EC in striatal synaptosomes (left side) and whole striatum (right side). SCOP behavioural effects were attenuated by cortical ablation, while those of APO were affected to a lesser extent. In the striatum of unoperated and sham-operated rats DHAA contents and DHAA/AA ratio resulted increased after drugs administration. No change in AA oxidation was observed in the striatum of ablated rats. In the synaptosomes of unoperated and sham-operated rats both drugs led to a decrease in DHAA contents and DHAA/AA ratio. In unoperated and sham-operated rats APO and SCOP caused a decrease of the DOPAC/DA ratio in the whole striatum and striatal synaptosmes. In ablated rats APO caused a decrease of DOPAC/DA ratio in the whole striatum and synaptosomes, while SCOP effects on DA turnover resulted attenuated in the whole striatum and abolished in synaptosomes. We conclude that drug-induced AA oxidation is likely to occur in the extracellular space and requires intact corticostriatal glutamatergic pathways. The latter may play an enabling role in SCOP behavioral effects.