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Abstract
Rat superfused striatal slices, preloaded with [3H]dopamine, were electrically stimulated
and the stimulation-induced outflow of radioactivity was taken as an index of dopamine
release. In the presence of 10 microM nomifensine, exposure of striatal slices to
unlabelled dopamine (0.3 microM) for 6 min prior to stimulation, significantly reduced
stimulation-induced outflow. In contrast, a 21-min exposure to dopamine did not significantly
alter stimulation-induced outflow. These results suggest that D2 receptors modulating
dopamine release in the rat striatum may be rapidly desensitized in vitro. Rats were
pretreated for 14 days with cocaine HCl (10 mg/kg/day i.p.) or saline. A progressive
enhancement of locomotor activity in cocaine-treated rats over the pretreatment period
compared to that in saline-treated rats indicated a behavioural sensitization to cocaine.
The inhibitory effect of pergolide (1, 10 and 100 nM) on stimulation-induced outflow
from striatal slices obtained from cocaine-pretreated rats was not different from
that in slices obtained from saline-pretreated rats. Therefore no evidence was obtained
for either a desensitization or a supersensitivity of striatal D2 autoreceptors by
chronic cocaine administration.