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Does nicotine affect D2 receptor upregulation? A case–control study
Author(s) -
Silvestri S.,
Negrete J. C.,
Seeman M. V.,
Shammi C. M.,
Seeman P.
Publication year - 2004
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.2004.00293.x
Subject(s) - downregulation and upregulation , nicotine , tardive dyskinesia , haloperidol , raclopride , medicine , receptor , dopamine receptor d2 , schizophrenia (object oriented programming) , endocrinology , pharmacology , psychology , dopamine , psychiatry , chemistry , biochemistry , gene
Objective: Nicotine has a powerful preventive effect on neuroleptic‐induced dopamine D2 receptor upregulation in the rat. The aim of this human positron emission tomography (PET) study was to compare upregulation in a smoker and a non‐smoker, both of whom had received haloperidol for the same duration of time. Method: Two subjects who had been treated for 16 years with a constant dose of haloperidol were scanned after temporary haloperidol withdrawal, using [ 11 C]‐raclopride. Results: The non‐smoker, who had received a dose of 10 mg/day, showed a D2 upregulation of 98% and developed severe and persistent symptoms of tardive dyskinesia (TD) upon withdrawal. The chronic smoker, who had been treated with 40 mg/day, displayed a D2 upregulation of 71% and did not develop TD. Conclusion: These human observations agree with animal data which showed that nicotine can decrease neuroleptic‐induced D2 receptor upregulation. This property of nicotine may play a protective role in movement disorders whose pathophysiology involves D2 receptor hypersensitivity.