Corticostriatal and thalamic regulation of amphetamine-induced ascorbate release in the neostriatum.
Lesions of cerebral cortex and ventromedial nucleus (VM) of the thalamus were made in rats to investigate the contribution of these structures to amphetamine (AMPH)-induced ascorbate (AA) release in the neostriatum as measured by in vivo voltammetry. Following a recovery period of at least one week, rats were anesthetized, and electrochemically modified, carbon-fiber electrodes were lowered into the neostriatum. Compared to data obtained from sham-operated and unoperated controls, bilateral aspiration lesions of cerebral cortex significantly lowered both the basal level of AA and the amount of AA released by AMPH in the neostriatum. Similar results were obtained after bilateral, but not unilateral electrolytic lesions of the VM thalamus. Collectively, these results suggest that the corticostriatal pathway and the VM thalamic nuclei participate in the regulation of basal and AMPH-induced AA release in the neostriatum.
Basse-Tomusk
A
A
Department of Psychology, Indiana University, Bloomington 47405.
Rebec
G V
GV
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D002421:Caudate Nucleus / Q000378:metabolism; D002540:Cerebral Cortex / Q000502:physiology*; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D003913:Dextroamphetamine / Q000494:pharmacology*; D004567:Electrodes, Implanted; D008297:Male; D011699:Putamen / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013788:Thalamus / Q000502:physiology*
D001205:Ascorbic Acid; D003913:Dextroamphetamine