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Related Experiment Videos

Does nicotine affect D2 receptor upregulation? A case-control study.

S Silvestri1, J C Negrete, M V Seeman

  • 1Centre for Addictions and Mental Health and Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.

Acta Psychiatrica Scandinavica
|March 11, 2004
PubMed
Summary

Nicotine may protect against antipsychotic side effects. In a study, a smoker on haloperidol had less dopamine D2 receptor upregulation and no movement disorder symptoms compared to a non-smoker.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Psychiatry

Background:

  • Neuroleptic medications, like haloperidol, can cause dopamine D2 receptor upregulation.
  • This upregulation is linked to movement disorders such as tardive dyskinesia (TD).
  • Animal studies suggest nicotine may prevent this neuroleptic-induced upregulation.

Observation:

  • This study investigated dopamine D2 receptor upregulation in a human smoker and non-smoker undergoing long-term haloperidol treatment.
  • Positron emission tomography (PET) with [11C]-raclopride was used to measure receptor availability after haloperidol withdrawal.

Findings:

  • The non-smoker (10 mg/day haloperidol) exhibited 98% D2 upregulation and developed severe tardive dyskinesia (TD).
  • The chronic smoker (40 mg/day haloperidol) showed 71% D2 upregulation and no TD symptoms.

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  • These findings align with animal data on nicotine's preventive effects.

    • Implications:

    • Nicotine's ability to reduce neuroleptic-induced D2 receptor upregulation may offer a protective role.
    • This could be significant for movement disorders associated with D2 receptor hypersensitivity.
    • Further research into nicotine's neuroprotective potential in psychiatric treatment is warranted.