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Acetylcholine, Tobacco Smoking, Genes

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Acetylcholine, Tobacco Smoking, Genes and Nicotinic Receptors

The purpose of the study is to measure the sensitivity of NCFHEB binding to changes in endogenous acetylcholine levels in healthy smoking and nonsmoking subjects, and in schizophrenic smoking and nonsmoking subjects. We hypothesize that physostigmine-induced elevated ACh levels will lead to a reduction in the availability of nicotinic receptors for the binding of the radioligand. We hypothesize there will be greater increase in ACh level (or greater reduction in radio tracer binding) in smoking as compared to nonsmoking subjects. We hypothesize there will be greater increase in ACh level (or greater reduction in radio tracer binding) in smoking as compared to nonsmoking subjects with schizophrenia, but the extent of this change will be different than in controls. We are also measuring the sensitivity of PHNO binding to changes in dopamine levels in healthy smoking and nonsmoking subjects before and after amphetamine challenge.

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Pharmaceutical medication involved common.study.methods.has-drugs-yes
Patients and healthy individuals accepted common.study.methods.is-healthy-no

Drug - Physostigmine

All subjects will receive physostigmine to induce elevated ACh levels in the brain.

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Acetylcholine, Tobacco Smoking, Genes and Nicotinic Receptors

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NCT02008292

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mepkrd