Long-term exposure to nicotine modulates the level and activity of acetylcholine receptors in white blood cells of smokers and model mice

Molecular Pharmacology
Anne CormierRegis Grailhe

Abstract

Long-term consumption of tobacco by smokers causes addiction and increases the level of neuronal nicotinic acetylcholine receptors (nAChRs) in the brain, a phenomenon known as up-regulation. Here, we show that up-regulation of specific nAChR subunits takes place in white blood cells (WBCs) of smokers and mice subjected to long-term administration of nicotine. The basal level of alpha-bungarotoxin binding site, which corresponds to the homomeric alpha7 nAChR subtype, was not affected in WBCs of both smokers and mice administered nicotine. In contrast, epibatidine (EB) binding sites, which correspond to heteromeric nAChR subtypes, were detected in WBCs of smokers but not in WBCs of nonsmokers. The number of EB binding sites significantly decreased after incubation of the smokers' WBCs for 3 days in nicotine-free culture medium. In WBCs of wild-type mice, basal level of EB binding sites was detected before nicotine administration. This basal level is reduced by approximately 60% in knockout mice lacking the genes encoding either the beta2 or the alpha4 receptor subunits. Additional analysis of knockout mice revealed that the remaining approximately 40% do not undergo up-regulation, indicating that the alpha4/beta2 subunits compris...Continue Reading

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Citations

Jul 17, 2008·The Journal of Infectious Diseases·Ilona A J GiebelenTom van der Poll
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