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Vol. 281, Issue 1, 508-513, 1997
Department of Pharmacology, Georgetown University School of
Medicine, Washington DC (S.R.T.),
Molecular Neuropsychiatry Section,
National Institutes of Health/National Institute on Drug Abuse,
Intramural Research Program, Baltimore, Maryland (B.L., J.L.C.)
Inhibition of dopamine (DA) transporter function is thought to be the
principal mechanism underlying cocaine's addictive effects. In
contrast to cocaine, several other inhibitors of DA transporter function are not considered to possess abuse liability. One of the
neuroadaptive changes to chronic cocaine self-administration is the
up-regulation of DA transporters. In the present study, we investigated
the reinforcing and neuroadaptive effects of two other DA reuptake
inhibitors, namely bupropion and nomifensine. Drug-naive rats readily
acquired and subsequently maintained consistent self-administration of
3 and 1 mg/kg/infusion doses of bupropion and nomifensine,
respectively, during 2-hr daily sessions over a prolonged period.
Similarly, self-administration responding at low doses of bupropion
(0.75 and 1.5 mg/kg/infusion) and nomifensine (0.1 and 0.3 mg/kg/infusion) showed some consistency during the initial weeks of
testing which gradually declined or tended to decline to levels similar
to that of the water control group during the later weeks of testing.
Bupropion self-administration dose-dependently up-regulated DA
transporters in caudate putamen and nucleus accumbens. In contrast,
nomifensine self-administration did not alter DA transporter levels.
These data provide evidence for heterogeneity among DA reuptake
inhibitors, with some of these drugs being able to up-regulate DA
transporters after their self-administration, whereas others lack this
neuroadaptive response.
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