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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.