Diseases related to tobacco use are prevalent throughout the world, resulting in more than 5 million deaths per year; in the US alone, annual tobacco-related mortality is ∼400,000 and annual healthcare costs are estimated at $96 billion. Nicotine is the primary psychoactive component of tobacco, triggering behavioral responses such as reward and anxiety reduction. Identifying the biochemical mechanisms that underlie nicotine-related behaviors may help us to develop new potential treatments for nicotine dependence or smoking cessation aids.
Nicotine works by interacting with various subtypes of nicotinic acetylcholine receptors (nAChRs), which are present in many brain pathways. Recent research has focused on narrowing down which specific receptors in which circuits underlie nicotine-induced behavioral responses. Now, Tresa M. McGranahan and colleagues at Salk Institute for Biological Sciences (La Jolla, CA) and University of Colorado (Boulder) report that blocking specific nAChRs containing α4 and β2 subunits on dopaminergic neurons in the brain decreases reward and anxiety-reduction behaviors in mice (J. Neurosci. 31, 10891–10902; 2011).
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