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Transcript
Nicotinic Acetylcholine Receptor Autoradiography After Chronic Cigarette Smoke Extract (CSE) or
Nicotine Exposure in Adult Male Rats
Michelle Cano
Mentors: Frances Leslie, Daisy Reynaga
Cigarette smoking carries many health risks and remains one of the most preventable causes of death in the
United States. Despite the adverse effects, many continue to smoke. The high addictive nature of smoking is
partially due to its main psychoactive component, nicotine. Nicotine acts by activating nicotinic acetylcholine
receptors (nAChRs). Post-mortem brains of smokers show upregulation of nAChRs, which is thought to play
a role in inducing dependence to smoking. Animals also show upregulation of nAChRs after chronic nicotine
exposure. However, these studies use nicotine alone to model tobacco dependence, ignoring the other 8,000
constituents found in cigarette smoke whose contribution to tobacco dependence have not been thoroughly
studied. Our lab has developed a preclinical model of tobacco dependence using cigarette smoke extract
(CSE), a saline solution containing nicotine and other aqueous non-nicotine constituents. In a preliminary
study, chronic CSE treatment resulted in enhanced somatic withdrawal when compared to nicotine alone in
adult male rats when precipitated with a non-selective nAChR antagonist, mecamylamine. The purpose of this
experiment is to determine if chronic CSE treatment results in a change in nAChR radioligand binding when
compared to nicotine alone. Preliminary results show trend drug differences in nAChR binding that are
subtype and region specific.