The effects of haloperidol, scopolamine, and MK-801 on amphetamine-induced increases in ascorbic and uric acid as determined by voltammetry in vivo.

Amphetamine (which enhances dopaminergic, cholinergic, and glutamatergic activity) increases release of ascorbic acid (AA) and uric acid (UA) in the caudate nucleus. In this study, linear sweep voltammetry with carbon past electrodes was used to investigate the effects of haloperidol (a DA receptor blocker), scopolamine (a muscarinic receptor blocker), and MK-801 (an NMDA receptor blocker) alone and in combination on amphetamine-induced increases in AA and UA in the caudate nucleus. Both scopolamine (0.5 mg/kg, IP) and MK-801 (0.5 mg/kg, IP) significantly reduced amphetamine-induced increases in AA. Also, scopolamine did not affect MK-801-induced reductions of amphetamine-induced increases in AA. Unexpectedly, a subthreshold dose of haloperidol (0.1 mg/kg, IP) potentiated the ability of scopolamine to block amphetamine-induced increases in AA. Therefore, the data suggest that acetylcholine release and subsequent binding to cholinergic receptors in the caudate, are components of amphetamine-induced increases in AA. In addition, scopolamine modulated haloperidol-induced reductions of amphetamine-induced increases in release of UA. Thus, our data demonstrate that cholinergic and dopaminergic systems may interact to control release of UA.