|dc.description.abstract||The problem. Nicotlne is an acetylcholine agonist that modulates the speed and efficiency
of information processing and attention. Recently, P300 event-related potentials (ERPs) have been utilized to examine the effects of nicotine and smoklng on brain activity and information
processing. These previous results indicate that nicotine decreases P300 latency and increases
P300 amplitude, indices which suggest faster and more efficient information processing. Nicotine's effect on P300 topography, to this date, has not been explored.
Procedure. The present study explored the effects of nicotine withdrawal on the latency, amplitude, and more specifically, the topography of the P300 ERP In withdrawn smokers (WS) withdrawn for 12 hours, nonwithdrawn smokers (NWS) and nonsmokers (NS) using a degraded visual continuous performance task (CPT). Signal detection analysis was applied, and behavioral measures of response bias (B"), perceptual sensitivity (A'), hit rate (HR), fake-alarm rate (FA), and median reaction time (RT) were examined.
Findings: Withdrawn smokers showed a decreased P300 amplitude relative to the NS and NWS groups, even after smoking. In contrast, there were no P300 latency differences between the three groups. A difference in P300 topography was revealed between the three groups as a group x electrode site interactlon using normalized P300 amplitudes. Two behavioral measures dlfferentiated between the three groups, HR and B", where the groups' responses varied as a function of session. Smokers, overall, tended to be statistically more conservative in their responses, preferring to commit the error of "miss" versus "false-alarms" relative to the nonsmokers. Nonsmokers overall possessed higher hit rates than smokers.||en