Effects of haloperidol on amphetamine-induced increases in ascorbic acid and uric acid as determined by voltammetry in vivo.
Amphetamine produces dramatic changes in extracellular ascorbic acid (AA) and uric acid (UA) in rat caudate; the origin of extracellular AA and UA is being widely investigated. In this study, linear sweep voltammetry with carbon paste electrodes was used to monitor extracellular AA and UA levels in conscious behaving rats. Amphetamine (2 and 4 mg/kg) produced a dose-related increase in UA; the increase in AA was very similar at both doses. Haloperidol (0.2 mg/kg) blocked the amphetamine-induced increase in UA but reduced the AA increase only by about 20%. Thus the amphetamine-induced increase in AA is only partly dependent on dopamine (DA) receptor stimulation whereas the amphetamine-induced increase in UA is completely dependent upon DA receptor stimulation.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D002421:Caudate Nucleus / Q000187:drug effects* / Q000378:metabolism; D003913:Dextroamphetamine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D006220:Haloperidol / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014527:Uric Acid / Q000378:metabolism*
D014527:Uric Acid; D006220:Haloperidol; D001205:Ascorbic Acid; D003913:Dextroamphetamine