Smoking motivation in normal subjects using event-related potentials

Abstract

The goal of the present study was to evaluate the effects of acute nicotine administration following 18 h of abstinence from cigarette smoking. Event-related potentials (ERPs) were measured in 13 male volunteers for five successive sessions. The peak amplitude and the area of the P300 significantly increased during acute withdrawal. An increase in P300 values also was observed following resumption of smoking. However, in subjects pretreated with nicotine gum, no increase in P300 values was observed following resumption of smoking. The increase in P300 values persisted for several weeks and returned to control values following 1 month of routine daily smoking. The P300 amplitude was negatively correlated with the daily dose of nicotine. These results suggest that attention and/or arousal may be enhanced by the withdrawal and the resumption of smoking. The mechanisms involved in CNS hypersensitivity to motivate the subject to smoke may persist in the presence of an increased P300 value, even following resumption of routine daily smoking.

Neuropsychology and neuropharmacology of P3a and P3b

“…Most ERP studies of tobacco smoking have focused on the acute rather than chronic effects of smoking. In general, P300 amplitude generally increases and latency decreases immediately after smoking (Houlihan et al, 1996(Houlihan et al, , 2002Knott et al, 1995a), although these effects appear relative to information processing task difficulty (Knott et al, 1995b;Pritchard and Robinson, 1998;Polich, 1999, 2001;Domino, 2003) and amount smoked as well as nicotine level (Kodama et al, 1996;Lindgren et al, 1999). The recent availability of de-nicotinized cigarettes should help to delineate this area, as previous studies typically employed non-smoking control subjects, "sham" smoking (pretending to inhale an unlit cigarette), or only pre-compared to post-smoking conditions in smokers.…”

Attention to novel and target stimuli in trauma survivors

“…In an early model of P300 amplitude, Johnson (1986) proposed “stimulus meaning” as one of the three primary determinants of P300 amplitude. Both before and after Johnson’s paper, P300 has been shown to be reliably larger to stimuli with high personal relevance and motivational value (Johnson et al, 1986; Berlad et al, 1995; Kodama et al, 1996; Gray et al, 2004; Ilardi et al, 2007; Goldstein et al, 2008). Such findings help explain the larger P300s to traumatic stimuli found in traumatized individuals with PTSD.…”

Acute nicotine fails to alter event‐related potential or behavioral performance indices of auditory distraction in cigarette smokers

“…The amplitude (reflecting attentional allocation) and latency (reflecting processing speed) of the parietal-central P300b component (peak latency ,300 ms)-elicited by correctly detected, low-probability target events in sensory discrimination task conditions-have been found to be decreased and prolonged, respectively, with smoking deprivation and are reversed, albeit not consistently, with acute smoking and nicotine administration (Domino, 2003;Edwards, Wesnes, Warburton, & Gale, 1985;Houlihan, Pritchard, & Robinson, 1996;Knott, Bosman, Mahoney, Ilivitsky, & Quirt, 1999;Knott, Harr, & Ilivitsky, 1996;Knott, Kerr, Hooper, & Lusk-Mikkelsen, 1995;Kodoma et al,1996). The limited number of distracter studies in the smoking-ERP literature, which generally have involved the presentation of task-irrelevant auditory stimuli interspersed among task-relevant auditory or visual target stimuli, have reported evidence of smoking-induced enhanced electrocortical habituation (reflected by reductions in P200 amplitudes) to distracters and diminished extended processing of distracters (reflected by amplitude reductions in a late, slow wave negative ERP component; Knott, 1985aKnott, , 1985bKnott et al, 1995).…”