Smoking Abstinence and Neurocognition: Implications for Cessation and Relapse

Abstract

In this chapter, we review the last decade of research on the effects of smoking abstinence on various forms of neurocognition, including executive function (working memory, sustained attention, response inhibition), reward processing, and cue-reactivity. In our review we identify smoking abstinence-induced deficits in executive function mediated by effects on frontal circuitry, which in turn is known to be affected by modulation of cholinergic, dopaminergic, and other neurotransmitter systems. We also review evidence that smoking abstinence blunts reactivity to non-drug reinforcers-a finding that is consistent with results in the animal literature. Finally, our review of cue-reactivity indicates that smoking abstinence does not appear to amplify cue-provoked craving, although it may increase attentional bias to smoking-related cues. Inconsistencies across findings and potential contributing factors are discussed. In addition, we review the literature on the effects of nicotine and non-nicotine factors in neurocognition. Finally, we provide a multi-factor model and an agenda for future research on the effects of smoking abstinence on neurocognition. The model includes four distinct yet interacting factors, including: Negative Reinforcement, Drug-Reward Bias, Goal and Skill Interference, and Non-Cognitive Factors. Additional research is needed to further evaluate the scope and time-course of abstinence-induced changes in neurocognition, the mechanisms that underlie these changes and the specific role of these processes in drug reinforcement, lapse, and relapse.

Brain CYP2B induction can decrease nicotine levels in the brain

“…In nicotine withdrawal, these receptors are unoccupied when nicotine is no longer present in the brain (De Biasi and Salas, 2008), possibly disrupting the activity of the neurotransmitter systems that express these receptors (Koob et al , 2004). Altered neurotransmitter activity in the absence of nicotine may be involved in the cognitive disturbances seen in withdrawal (McClernon et al , 2015) and subsequent nicotine intake may be a response to alleviate these symptoms (Koob et al , 2004). If brain CYP2B induction occurs along with these adaptive receptor and neurotransmitter changes, lower brain nicotine levels may lead to insufficient activation of the nAchRs, which could reduce nicotine’s attenuation of withdrawal symptoms.…”

Transdiagnostic impairment of cognitive control in mental illness

“…Diamond, 2013 for review). Even among healthy individuals, cognitive control capacity predicts endeavors and success in educational performance and attainment (Duncan et al, 2007), occupational stability and advancement (Foxall, 2014), health promotion (McClernon et al, 2015; Riggs et al, 2010), as well as broader measures of overall quality of life (Davis et al, 2010). Given the influence on functional status among healthy individuals, cognitive control/executive functions are likely integral to the development, resistance to, maintenance, and remediation of psychopathology.…”

Nicotine withdrawal-induced inattention is absent in alpha7 nAChR knockout mice

“…Patients report difficulty concentrating and confusion with quantified nicotine withdrawal-induced impairments to working memory, attention, response inhibition, reward processing, and reaction time (Hughes 2007; McClernon et al 2015; van Enkhuizen and Young 2016). In fact, some of these cognitive impairments, including attention deficits and impulse control, before and during withdrawal can predict relapse (Pomerleau et al 2003; Dolan et al 2004; Rukstalis et al 2005; Krishnan-Sarin and Reynolds 2007; Culhane et al 2008; Powell et al 2010).…”

“…In this study, we assessed the cognitive deficits associated with nicotine withdrawal in healthy mice and those lacking α7 nAChRs, hypothesizing, based on rat and human studies (Shoaib and Bizarro 2005; Semenova et al 2007; Harrison et al 2009; McClernon et al 2015), that attention would be disrupted during withdrawal. Furthermore, we hypothesized that mice lacking α7 nAChRs would not exhibit nicotine withdrawal-induced deficits in attention.…”