Reduction of withdrawal signs after chronic nicotine exposure of alpha-calcitonin gene-related peptide knock-out mice

Neurosci Lett. 2004 Apr 22;360(1-2):73-6. doi: 10.1016/j.neulet.2004.02.031.


Nicotine, the main substance responsible for the addictive behavior of smokers, binds to a variety of nicotinic acetylcholine receptors (nAChRs) diversely distributed in the brain, notably in areas involved in motivation and reward mechanisms. The alpha-calcitonin gene-related peptide (alphaCGRP) has been previously shown to modulate the functions of nAChRs and is released in brain areas implicated in motivation, such as the amygdala or the ventral tegmental area. Interestingly, alphaCGRP -/- mice display a decrease in morphine withdrawal symptoms. In this context, we investigate the tolerance and withdrawal symptoms in alphaCGRP -/- mice exposed to acute and chronic nicotine. We report that these animals develop a normal tolerance to the antinociceptive effects of nicotine, but display an attenuation of somatic withdrawal symptoms.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcitonin Gene-Related Peptide / deficiency*
  • Calcitonin Gene-Related Peptide / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nicotine / administration & dosage*
  • Substance Withdrawal Syndrome / genetics
  • Substance Withdrawal Syndrome / metabolism*
  • Tobacco Use Disorder / genetics
  • Tobacco Use Disorder / metabolism*


  • Nicotine
  • Calcitonin Gene-Related Peptide