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Research ArticleBehavioral Pharmacology

Nicotine Reduces Antipsychotic-Induced Orofacial Dyskinesia in Rats

Tanuja Bordia, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics March 2012, 340 (3) 612-619; DOI: https://doi.org/10.1124/jpet.111.189100
Tanuja Bordia
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J. Michael McIntosh
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Maryka Quik
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Abstract

Antipsychotics are an important class of drugs for the management of schizophrenia and other psychotic disorders. They act by blocking dopamine receptors; however, because these receptors are present throughout the brain, prolonged antipsychotic use also leads to serious side effects. These include tardive dyskinesia, repetitive abnormal involuntary movements of the face and limbs for which there is little treatment. In this study, we investigated whether nicotine administration could reduce tardive dyskinesia because nicotine attenuates other drug-induced abnormal movements. We used a well established model of tardive dyskinesia in which rats injected with the commonly used antipsychotic haloperidol develop vacuous chewing movements (VCMs) that resemble human orofacial dyskinesias. Rats were first administered nicotine (minipump; 2 mg/kg per day). Two weeks later, they were given haloperidol (1 mg/kg s.c.) once daily. Nicotine treatment reduced haloperidol-induced VCMs by ∼20% after 5 weeks, with a significant ∼60% decline after 13 weeks. There was no worsening of haloperidol-induced catalepsy. To understand the molecular basis for this improvement, we measured the striatal dopamine transporter and nicotinic acetylcholine receptors (nAChRs). Both haloperidol and nicotine treatment decreased the transporter and α6β2* nAChRs (the asterisk indicates the possible presence of other nicotinic subunits in the receptor complex) when given alone, with no further decline with combined drug treatment. By contrast, nicotine alone increased, while haloperidol reduced α4β2* nAChRs in both vehicle and haloperidol-treated rats. These data suggest that molecular mechanisms other than those directly linked to the transporter and nAChRs underlie the nicotine-mediated improvement in haloperidol-induced VCMs in rats. The present results are the first to suggest that nicotine may be useful for improving the tardive dyskinesia associated with antipsychotic use.

Footnotes

  • This work was supported by the National Institutes of Health National Institute of Neurological Disorders and Stroke [Grants NS47162, NS59910]; and the National Institutes of Health National Institute of Mental Health [Grant MH53631].

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

    http://dx.doi.org/10.1124/jpet.111.189100.

  • ABBREVIATIONS:

    DA
    dopamine
    DAT
    DA transporter
    VCMs
    vacuous chewing movements
    RTI-121
    3β-(4-iodophenyl)tropane-2β-carboxylic acid isopropyl ester
    α-CtxMII
    α-conotoxin MII
    ANOVA
    analysis of variance
    nAChRs
    nicotinic acetylcholine receptors (the asterisk indicates the possible presence of other nicotinic subunits in the receptor complex)
    CNS
    central nervous system.

  • Received October 17, 2011.
  • Accepted December 5, 2011.
  • Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 340 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 340, Issue 3
1 Mar 2012
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Research ArticleBehavioral Pharmacology

Nicotine and Tardive Dyskinesia

Tanuja Bordia, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics March 1, 2012, 340 (3) 612-619; DOI: https://doi.org/10.1124/jpet.111.189100

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Research ArticleBehavioral Pharmacology

Nicotine and Tardive Dyskinesia

Tanuja Bordia, J. Michael McIntosh and Maryka Quik
Journal of Pharmacology and Experimental Therapeutics March 1, 2012, 340 (3) 612-619; DOI: https://doi.org/10.1124/jpet.111.189100
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