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Vol. 282, Issue 1, 7-13, 1997
Denver Veterans Administration Medical Center (J.L., S.L.) and
Department of Psychiatry (C.R.B., C.E.A., B.S., S.L.), University of
Colorado Health Sciences Center, Denver, Colorado and
Institute for
Behavioral Genetics, Department of Psychology (M.J.M., A.C.C.),
University of Colorado, Boulder, Colorado
Chronic nicotine administration in animal models evokes a
dose-dependent increase in brain nicotinic receptor numbers.
Genetically determined variability in nicotinic receptor number in
different mouse strains has also been reported, which is thought to
affect sensitivity to nicotine, as well as the development of
tolerance. Humans self-administer nicotine principally in the form of
cigarettes and other tobacco products. The present study compared
[3H]nicotine binding in human postmortem brain from
thalamus and hippocampus of nonsmoking subjects, subjects who had
variable life-long smoking histories and subjects who had quit smoking. A significant increase was seen in [3H]nicotine binding
in both hippocampus and thalamus of subjects with life-long smoking
histories. In the hippocampus, this change resulted from a change in
total receptor number (Bmax), with no change
in receptor affinity (Kd). There was also a
positive correlation between the degree of smoking, as measured by the
average reported packs smoked per day, and the number of nicotine
binding sites found in both the hippocampus and thalamus, showing that
humans exhibit a dose-dependent increase in brain nicotinic receptor binding. Receptor levels in these brain regions after smoking cessation
were at or below those found in the control population, which indicated
that smoking-induced changes are reversible after cessation of nicotine
treatment. These results suggest that increases in nicotinic receptor
levels in the human brain may underlie nicotine tolerance and addiction
in smokers.
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