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The Journal of Neuroscience, August 15, 2001, 21(16):6338-6347
Preferential Increases in Nucleus Accumbens Dopamine after
Systemic Cocaine Administration Are Caused by Unique Characteristics of
Dopamine Neurotransmission
Qun
Wu1,
Maarten E. A.
Reith2,
Michael J.
Kuhar3,
F. Ivy
Carroll4, and
Paul A.
Garris1, 2
1 Cellular and Integrative Physiology Section,
Department of Biological Sciences, Illinois State University, Normal,
Illinois 61790-4120, 2 Department of Biomedical and
Therapeutic Sciences, University of Illinois College of Medicine at
Peoria, Peoria, Illinois 61656-1649, 3 Neuroscience
Division, Yerkes Regional Primate Research Center, Emory University,
Atlanta, Georgia 30322, and 4 Chemistry and Life Sciences,
Research Triangle Institute, Research Triangle Park, North Carolina
27709-9981
In vivo voltammetry was used to investigate the
preferential increase of extracellular dopamine in the nucleus
accumbens relative to the caudate-putamen after systemic cocaine
administration. In the first part of this study, cocaine (40 mg/kg,
i.p.) was compared with two other blockers of dopamine uptake,
nomifensine (10 mg/kg, i.p.) and
3 -(p-chlorophenyl)tropan-2-carboxylic acid p-isothiocyanatophenylmethyl ester hydrochloride
(RTI-76; 100 nmol, i.c.v.), to assess whether the inhibitory mechanism
of cocaine differed in the two regions. All three drugs robustly
increased electrically evoked levels of dopamine, and cocaine elevated
dopamine signals to a greater extent in the nucleus accumbens. However, kinetic analysis of the evoked dopamine signals indicated that cocaine
and nomifensine increased the Km for
dopamine uptake whereas the dominant effect of RTI-76 was a decrease in
Vmax. Under the present in vivo
conditions, therefore, cocaine is a competitive inhibitor of dopamine
uptake in both the nucleus accumbens and caudate-putamen. Whether the
preferential effect of cocaine was mediated by regional differences in
the presynaptic control of extracellular DA that are described by rates
for DA uptake and release was examined next by a correlation analysis.
The lower rates for dopamine release and uptake measured in the nucleus accumbens were found to underlie the preferential increase in extracellular dopamine after cocaine. This relationship explains the
paradox that cocaine more effectively increases accumbal dopamine despite identical effects on the dopamine transporter in the two regions. The mechanism proposed for the preferential actions of cocaine
may also mediate the differential effects of psychostimulant in
extrastriatal regions and other uptake inhibitors in the striatum.
Key words:
cocaine; dopamine; caudate-putamen; nucleus accumbens; voltammetry; uptake
Copyright © 2001 Society for Neuroscience 0270-6474/01/21166338-10$05.00/0
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