(Ettinger et al., 2009). Nicotine administered to non-smokers decreases DMN activity “at rest” (Fig 4C; Tanabe et al., 2011), suggesting such effects are not constrained to task-specific contexts nor limited to the amelioration of abstinence-induced effects in smokers. In contrast to nicotine-induced decreases in DMN and consistent with enhancement of sensory-based information processing, nicotine potentiates rsFC in cingulate-neocortical circuits of minimally-deprived smokers (Fig 2A; Hong et al., 2009) and in extrastriate visual circuits of non-smokers (Tanabe et al., 2011). Such nicotine-induced suppression of DMN and reciprocal enhancement of TPN activity at the systems-level, may parallel acetylcholine’s role in toggling circuit dynamics between cortico-cortical feedback states (low acetylcholine levels) and thalamo-cortical feed-forward states (high acetylcholine levels) described at the cellular-level (Hasselmo and McGaughy, 2004; Bentley et al., 2011).
