Acetylcholine is involved in cognitive processes, and the ability of nicotine to modulate nicotinic acetylcholinergic receptor function contributes to the effects of tobacco on learning and other cognitive processes. The capacity of nicotine to alter learning and cognition may facilitate the development and maintenance of nicotine addiction. Nicotine may enhance the formation of strong but yet maladaptive drug-stimuli associations that can trigger cravings and drug-seeking behavior upon reexposure to the stimuli. In addition, defi cits in cognition during periods of abstinence may contribute to smoking relapse. Nicotine may initially alter cellsignaling cascades involved in learning and synaptic plasticity to facilitate cognition, but continued use may lead to compensatory adaptations in nicotinic receptor function, such as receptor desensitization and upregulation that contribute to tolerance and withdrawal defi cits in cognition. The effects of nicotine on cognition are infl uenced by the brain regions involved in the cognitive tasks and by both genetics and developmental stage.
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