The etiology of nicotine addiction involves a

The etiology of nicotine addiction involves a complex interplay between genetic predisposition and environmental factors (reviewed in Ray et al., 2009). It is reasonable to expect that individual differences in the liability to nicotine addiction are mediated by relatively distinct neurocognitive processes involved in reward learning and self-regulation of behavior, all of which contribute to the risk for addiction in both additive and interactive way. Identification and characterization of the unique role of each of these “component processes” in addictive behaviors and elucidation of their genetic basis is needed for building an integrative model of addiction. It is important to note that the etiology of addictions is a dynamic process that involves distinct stages such as initiation of drug use, progression to regular use, and the development of dependence on the drug. In particular, genetic factors influencing the risk for initiation of tobacco use appear to be distinct from those affecting progression to regular smoking and nicotine dependence (Heath et al., 2002; Munafo et al., 2004), suggesting distinct underlying biological liability. However, little is known about specific neurocognitive mechanisms operating at different stages of substance involvement. One of the neurocognitive component processes contributing to addiction risk may be error monitoring, a fundamental mechanism of self-regulation of behavior that involves automatic, largely pre-conscious detection of the mismatch between the intended and actually executed action and subsequent cognitive and emotional appraisal of the detected conflict prompting the recruitment of cognitive control for adjustments of ongoing behavior (Segalowitz and Dywan, 2009; van Noordt and Segalowitz, 2012). These stages of error processing are reflected in ERP components associated with commission of errors, the error-related negativity (ERN) and error positivity (P) depicted in Fig. 1. Converging evidence from studies using ERP source localization analyses, multimodal imaging (EEG and fMRI), single unit recording, and studies of patients with rxr receptor lesions indicates that the main anatomical source of ERN is the anterior cingulate cortex (Debener et al., 2005; Herrmann et al., 2004; Mathalon et al., 2003; Miltner et al., 2003; Ridderinkhof et al., 2004). A previous study in our laboratory has demonstrated significant heritability of individual differences in ERN and P components, suggesting that ERN can serve as an endophenotype for disorders characterized by self-regulation deficits (Anokhin et al., 2008). Over the past decade, ERN has been increasingly used in the investigation of neurocognitive mechanisms mediating the risk for psychopathology, including addictive disorders. A thorough review of these studies is beyond the scope of this introduction and we refer the reader to comprehensive reviews on this topic (Moser et al., 2013; Olvet and Hajcak, 2008; van Noordt and Segalowitz, 2012). Briefly, this evidence suggests that increased ERN, presumably indicating abnormally over-active error monitoring system, is associated with obsessive–compulsive, depressive and anxiety-spectrum symptomatology (Aarts et al., 2013b), whereas reduced ERN is associated with personality traits indicating impulsivity, poor socialization, and externalizing symptoms in children and adults (Dikman and Allen, 2000; Hall et al., 2007; Santesso et al., 2005; Stieben et al., 2007). These correlations with psychopathology are broadly consistent with the notion that ERN reflects not only cognitive but also emotional processing of errors (Aarts et al., 2013a; Koban and Pourtois, 2014). Given this pattern of findings, it is reasonable to hypothesize that deficits in the neural mechanisms of error monitoring may contribute to poor self-regulation of behavior and thus increase the risk for initiation of substance use in adolescents. In particular, a large portion of adolescents (>40%) initiate tobacco use by age 18, despite increasing public awareness of substantial health risks associated with smoking and overall decline in smoking rates. One potential mechanism mediating the hypothesized link between poor action monitoring and tobacco use is impulsivity. This hypothesis is supported by three lines of evidence. First, adolescent smokers tend to score higher on laboratory and self-repot measures of impulsivity (Reynolds et al., 2007), and impulsivity is one of important prospective predictors of smoking initiation in adolescence (O’Loughlin et al., 2014). Second, studies reported associations between reduced ERN and higher impulsivity (Potts et al., 2006), broader externalizing and impulse-control problems (Hall et al., 2007), ADHD (Shiels and Hawk, 2010), and risk-taking (Santesso and Segalowitz, 2009). Third, developmental neuroscience has demonstrated that the brain continues to develop during adolescence. Areas of the prefrontal cortex supporting behavioral regulation are characterized by the longest development lasting into the young adulthood, and their relative immaturity may be responsible for poorer self-regulation of behavior in adolescents compared with adults (Casey et al., 2008; Richards et al., 2012; Spear, 2013). These lines of evidence converge to suggest that the neural mechanisms of action monitoring may be immature and continue to develop during adolescence, and individuals with slower or attenuated development may be more prone to impulsive and risky actions such as experimenting with tobacco and other drugs.