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Positron emission tomography to quantify brain nicotine abstinence
Author(s) -
Domino E. F.,
Tsukada H.
Publication year - 2005
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2005.01.003
Subject(s) - nicotine , abstinence , striatum , ventral striatum , raclopride , dopamine , medicine , anesthesia , pharmacology , psychology , psychiatry
Background The hypothesis for this research was that brain dopamine (DA) utilization would decrease during abstinence from repeated nicotine administration. Methods Six young Macaca mulatta monkeys were given 0.9% NaCl or nicotine in doses of 32 or 100 μg/kg i.m. bid for 9 days. On the 10th day, PET measurements were repeated before and after nicotine. The PET studies were done in habituated, trained, and fully conscious animals. Results Compared to the control condition, the binding potential (k3/k4) of[11C]raclopride in dorsal or ventral striatum did not change with either dose following acute repeated nicotine, or in the nicotine abstinent state. Compared to control, acute nicotine in either dose did not affect the DA utilization rate constant (k3) in dorsal or ventral striatum as measured by[Beta‐11C]L‐DOPA. However, in monkeys given nicotine repeatedly, after overnight nicotine abstinence, DA utilization was reduced significantly. A subsequent nicotine dose increased DA utilization to slightly above control levels. The ventral striatum showed greater changes than the dorsal striatum. Conclusions The reduced rate of DA synthesis as assayed with[Beta‐11C]L‐DOPA during nicotine abstinence and its reversal by nicotine provides an important PET measure of brain nicotine dependence and withdrawal. Clinical Pharmacology & Therapeutics (2005) 77 , P98–P98; doi: 10.1016/j.clpt.2005.01.003