CORTICOLIMBIC FUNCTIONING, NICOTINE DEPENDENCE CHARACTERISTICS, AND SMOKING LAPSE HISTORY: AN FMRI STUDY
Publication or External Link
Nicotine dependence is a prevalent and costly disorder characterized by notoriously high relapse rates. Extant research implicates stress as a key mechanism driving smoking across the stages of addiction, and neurobiological models of stress and addiction emphasize the role of overlapping corticolimbic circuits in both emotion dysregulation and compulsive drug seeking. However, neuroimaging research examining the neural correlates of stress processing in human smokers is limited and lacking in some areas, leaving key questions unanswered. Specifically, it is unclear how neural responses to stress may explain individual differences in nicotine dependence severity and cessation attempt outcomes. Moreover, more recent theoretical and empirical work has highlighted the importance of looking beyond functioning in discreet neural regions and has emphasized the importance of examining how brain functioning at a network level, through the use of resting state functional connectivity, might explain addictive behavior. However, research examining the relationship between functional connectivity and clinically-relevant smoking measures is also limited. As a first step toward addressing these gaps in the literature, the current study utilized a novel fMRI-compatible psychological stress induction task to examine the relationships between stress-induced neural activation, as well as resting state functional connectivity within stress-related corticolimbic circuits, and clinically-relevant smoking characteristics among a sample of adult cigarette smokers. Analysis of the fMRI data collected during administration of the novel stress induction task revealed significant stress-induced activation in the right insula, a region previously implicated in the interoceptive experience of negative affective states, as well as visceral symptoms of nicotine withdrawal and craving. Contrary to expectations, there were no significant relationships identified between stress-induced neural functioning, or functional connectivity within stress-related circuits, and the clinically-relevant smoking measures that were assessed. Findings are discussed in light of several study limitations and directions for future research are enumerated.