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Research ArticleNeuropharmacology

Long-Term Nicotine Exposure Depresses Dopamine Release in Nonhuman Primate Nucleus Accumbens

Xiomara A. Perez, Jason Ly, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics August 2012, 342 (2) 335-344; DOI: https://doi.org/10.1124/jpet.112.194084
Xiomara A. Perez
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Jason Ly
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J. Michael McIntosh
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Maryka Quik
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Abstract

Tobacco use is a leading cause of preventable deaths worldwide. However, current smoking cessation therapies have very limited long-term success rates. Considerable research effort is therefore focused on identification of central nervous system changes with nicotine exposure because this may lead to more successful treatment options. Although recent work suggests that α6β2* nicotinic acetylcholine receptors (nAChRs) play a dominant role in dopaminergic function in rodent nucleus accumbens, the effects of long-term nicotine exposure remain to be determined. Here, we used cyclic voltammetry to investigate α6β2* nAChR-mediated release with long-term nicotine treatment in nonhuman primate nucleus accumbens shell. Control studies showed that nAChR-mediated dopamine release occurs predominantly through the α6β2* receptor subtype. Unexpectedly, there was a complete loss of α6β2* nAChR-mediated activity after several months of nicotine treatment. This decline in function was observed with both single- and multiple-pulse-stimulated dopamine release. Paired-pulse studies showed that the facilitation of dopamine release with multiple pulsing observed in controls in the presence of nAChR antagonist was lost with long-term nicotine treatment. Nicotine-evoked [3H]dopamine release from nucleus accumbens synaptosomes was similar in nicotine- and vehicle-treated monkeys, indicating that long-term nicotine administration does not directly modify α6β2* nAChR-mediated dopamine release. Dopamine uptake rates, as well as dopamine transporter and α6β2* nAChRs levels, were also not changed with nicotine administration. These data indicate that nicotine exposure, as occurs with smoking, has major effects on cellular mechanisms linked to α6β2* nAChR-mediated dopamine release and that this receptor subtype may represent a novel therapeutic target for smoking cessation.

Footnotes

  • This work was supported by the National Institutes of Health National Institute of Neurological Disorders and Stroke [Grant NS59910]; the National Institutes of Health National Institute of Mental Health [MH53631]; the National Institutes of Health National Institute of General Medical Sciences [GM48677]; and the California Tobacco Related Disease Research Program [Grant 17RT-0119].

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

    http://dx.doi.org/10.1124/jpet.112.194084.

  • ABBREVIATIONS:

    nAChR
    nicotinic acetylcholine receptor
    α-CtxMII
    α-conotoxin MII
    RTI-121
    3β-(4-iodophenyl)tropane-2β-carboxylic acid.

  • Received March 7, 2012.
  • Accepted May 3, 2012.
  • Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 342 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 342, Issue 2
1 Aug 2012
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Research ArticleNeuropharmacology

Long-Term Nicotine Depresses Dopamine Release

Xiomara A. Perez, Jason Ly, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics August 1, 2012, 342 (2) 335-344; DOI: https://doi.org/10.1124/jpet.112.194084

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Research ArticleNeuropharmacology

Long-Term Nicotine Depresses Dopamine Release

Xiomara A. Perez, Jason Ly, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics August 1, 2012, 342 (2) 335-344; DOI: https://doi.org/10.1124/jpet.112.194084
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