During acute nicotine withdrawal, smokers often report subjectively experienced “difficulty concentrating” and display objectively assessed impairments in task-based performance (Heishman 1998; Hendricks et al., 2006; Kozink et al., 2010). In keeping with the dynamic network view discussed above, increased DMN functioning, decreased TPN operations, and/or maladaptive interactions between components of these networks may account for abstinence-induced cognitive impairments. Supporting such a proposal, self-reported improved concentration following nicotine administration to abstinent smokers has been associated with increased negative coupling between DMN and TPN regions (Fig 4D; Cole et al., 2010). Additionally, nicotine decreases intra-individual response time variability (Hahn et al., 2007); variability thought to arise from maladaptive dynamic interactions between DMN and TPN (Kelly et al., 2008). Relative to the drug-sated state, 24-hr abstinence leads to reduced activation in TPN regions (e.g. lateral PFC) during performance of a sustained attention task (Ettinger et al., 2009). Nicotinic stimulation with varenicline, a modestly efficacious pharmacotherapy for smoking cessation, increases activity in core TPN nodes (i.e., lateral and posterior-medial PFC) during demanding working memory performance following smoking abstinence (Loughead et al., 2011). Thus, we
