Abstract
Tobacco addiction is characterized by compulsive smoking and negative affective withdrawal signs upon smoking cessation. Animal studies have started to explore the neuronal mechanisms that mediate anxiety-like behavior associated with nicotine withdrawal. These studies show that cessation of prolonged noncontingent nicotine administration leads to an increase in anxiety-like behavior in rats and mice. Cessation of long-access (>21h/day) nicotine self-administration, but not short-access (1h/day) nicotine self-administration, also leads to an increase in anxiety-like behavior. Nicotine-induced changes in corticotropin-releasing factor (CRF) transmission play a role in nicotine withdrawal. Recent studies have shown that blockade of CRF type 1 receptors and stimulation of CRF type 2 receptors diminish anxiety-like behavior associated with nicotine withdrawal. Overall, these studies indicate that rodents display increased anxiety-like behavior upon cessation of contingent and noncontingent nicotine administration, and these effects are partly mediated by nicotine-induced changes in CRF transmission in the brain.
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