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Nonaffective constraint is a personality trait concerned with the modulation of activity in motor, emotional, and cognitive domains.
Nonaffective constraint (NC) is a personality trait with roots in both neuroscience and personality research. Depue and Collins (1999) first conceptualized NC as a neuroregulatory system that modulates activity in motor, emotional, and cognitive domains. High levels of NC allows for greater levels of control over reactive behaviors, emotions, and cognitions (Depue and Lenzenweger 2015; Moore and Depue 2016). Rooted in a threshold model of behavioral reactivity, NC assumes a central neural contribution for such inhibition (see below). While there is no single neurobiological correlate for NC, self-report and neurocognitive tasks are well established in measuring NC at the behavioral level. Self-report instruments such as the constraint scale within the Multidimensional Personality Questionnaire (Tellegen 1982) assesses aspects of NC as well. Neurocognitive tasks such as the Go-No Go Task (Goldstein et al. 2007) and the Wisconsin Card Sorting Tasks (Heaton et al. 1993) represent performance-based measures of aspects of NC. The closest neighbor personality trait in the Five Factor Model to NA is Conscientiousness. However, Conscientiousness and NC have significant conceptual differences as well. Further, Conscientiousness is not rooted in basic neuroscience findings and includes elements of moral values and perfectionism not that are not central to NA.
Breakdowns in NA contribute to various forms of psychopathology, particularly through the trait of impulsivity, or, impaired NC (Eysenck and Eysenck 1977; Tellegen and Waller 1997). Attention Deficit Hyperactivity Disorder (Nigg 2001), substance use disorders (Jentsch and Taylor 1999), personality disorders (particularly borderline personality disorder) (Fertuck et al. 2005, 2006; Lenzenweger et al. 2004; Perez et al. 2016) and schizophrenia (Gut-Fayand et al. 2001) all exhibit impairments in NA in some form and degree. There is preliminary research indicating that effective treatment for borderline personality disorder is associated with improvement in NC at behavioral and neurofunctional levels (Perez et al. 2016). This increased NA was reflected in increased activity in prefrontal regions and decreased reactivity of fear processing regions (i.e., the amygdala) that occur in conjunction with symptom reduction.
Neurochemically, early animal models pointed to serotonergic pathways as possible neurochemical source of NC (Depue and Collins 1999), as serotonin depletion often triggers loss of behavioral inhibition (Spoont 1992). However, when NC is conceptualized as a more general inhibitory mechanism (Bari and Robbins 2013), recent evidence using the stop-signal task (which requires the withholding of prepotent responses) (Logan 1982, 1983) suggests that noradrenergic pathways predominate (Aston-Jones and Cohen 2005; Aston-Jones et al. 1999; Berridge and Waterhouse 2003; Sara 2009; Yu and Dayan 2005), especially for inhibition of behaviors already activated (Eagle et al. 2008; Robbins and Arnsten 2009), with only a minor contribution of the serotonergic system (Clark et al. 2005; Nandam et al. 2011; Overtoom et al. 2009). A recent suggestion (Aron 2011) divides NC into a reactive process that directly halts activated responses, perhaps noradrenergic through the involvement of the locus coeruleus and a proactive process that inhibits behaviors selectively, perhaps through the dopaminergic involvement of the striatum (Boehler et al. 2011).
Neuroanatomically, the executive management of NC is the purview of the prefrontal cortex (PFC). Here, a division of labor is evident, with motor inhibition controlled by the supplementary motor area (SMA) and pre-SMA (Aron and Poldrack 2006; Fried et al. 1991; Li et al. 2006), distractor and emotional inhibition controlled by the dorsolateral PFC (Delgado et al. 2008), and the monitoring of errors and conflict of competing responses by the anterior cingulate cortex (Botvinick et al. 2001; Holroyd and Coles 2002). Inhibitory control is seen as hierarchical, with PFC affecting a variety of cortical and subcortical brain regions through its projections to amygdala, hypothalamus, basal ganglia, premotor cortex, cingulate cortex, and posterior parietal cortex. Although originally conceived as a stable feature of the central nervous system, NC is amenable to neural plasticity, revealing long-lasting enhancements in inhibitory control following cognitive training interventions (Eldar and Bar-Haim 2010; Melara et al. 2002).
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