We tested the hypothesis that some of the intoxicating effects of ethanol could be due to action of its metabolite, acetaldehyde. Single-unit impulse activity from cerebellar cortex was compared between two groups of rats given ethanol intravenously (0.64 g/kg). In one group accumulation of acetaldehyde was prevented by pre-treatment with d-penicillamine (1.2 g/kg) which is known to prevent acetaldehyde build-up as ethanol is metabolized. Both the discharge rate and the interval histogram distribution in both groups were comparable before ethanol administration, indicating that penicillamine had no effect of its own. Similar effects of ethanol were seen in both test groups, thus failing to indicate that acetaldehyde accounts for ethanol-induced changes in unit activity.