It has been reported that ascorbic acid (AA) antagonizes the physiological
and behavioral effects of dopamine (DA). AA reduces locomotor activity indu
ced by dopaminergic agonist drugs. Also, AA amplifies the action of antidop
aminergic drugs. Ethanol, like other drugs, produces a release of DA in the
mesolimbic pathway, and at some doses, induces locomotor activity in mice.
The ethanol-induced locomotor activity could be dopamine-dependent because
it can be reduced by antidopaminergic drugs. In the present study, we inve
stigated whether an acute administration of AA reduces ethanol-induced loco
motor behavior. AA, at doses (0.0, 21.85, 87.5, 175, 350, and 1400 mg/kg) w
as injected IP into mice, 0, 30, 60, or 90 min before an IP injection of et
hanol (0.0, 0.8, 1.6, 2.4, and 3.2 g/kg). Locomotor activity was evaluated
in open-field chambers. Our results showed that AA (350 and 1400 mg/kg) red
uced ethanol-induced locomotor activity when injected 30 min before ethanol
treatment. This effect was lost when ethanol was administered 90 min after
AA injection. AA also reduced locomotor activity produced by d-amphetamine
and methanol. The results support a pro-dopaminergic action of ethanol, an
d suggest a common dopaminergic pathway for the drugs of abuse in locomotor
activity. (C) 1999 Elsevier Science Inc.