Tiffany Wallace

We identified a potential novel site of action for nicotine since a) systemic injection of nicotine led to a dose-dependent decrease in the amplitude of the sleep state-dependent, vertex-recorded, P13 midlatency auditory evoked potential, which is generated by the reticular activating system (RAS), b) localized injections of a nicotinic receptor antagonist into the cholinergic arm of the RAS, the pedunculopontine nucleus (PPN), blocked the effects of systemic nicotine on the P13 potential, a measure of level of arousal, and c) localized injection of a nicotinic receptor agonist into the PPN also led to a decrease in the amplitude of the P13 potential, an effect blocked by PPN injection of a nicotinic receptor antagonist.  There were minor changes in the manifestation of the startle response (SR) at the concentrations used, however, nicotine did decrease the hippocampal N40 potential, although its effects were not affected by antagonist or agonist injections into the PPN.  These results suggest a potential mechanism underlying the anxiolytic effects of nicotine, i.e. suppression of the cholinergic arm of the RAS.


These results may account for the excessive smoking seen in mental disorders such as schizophrenia, anxiety disorders and depression, all marked by hypervigilance.  These patients may be using smoking to self-medicate with nicotine in order to induce an anxiolytic effect, however brief, prompting chain smoking.