Finally, there is some evidence to suggest that the state-dependent changes in impulse control function in bipolar disorder involve altered catecholamine and, in particular, altered noradrenaline activity. As noted previously, administration of atomoxetine has been shown repeatedly to modulate action cancellation as measured in the Stop-Signal task (Bari et al., 2009; Chamberlain et al., 2006, 2007; Eagle et al., 2008; Schachar et al., 2001). Other data have shown comparable results following desipramine treatment (Overtoom et al., 2003). Noradrenaline has a profound influence on the cognitive functions of the prefrontal cortex function mediated by a balance of α-1 and α-2 adrenoceptor activity (Arnsten et al., 1999). Under conditions of extreme stress, excessive stimulation of α-1 adrenoceptors can impair prefrontal cortical cognitive activity. Other situations that elicit noradrenaline release, such as manic states in bipolar disorder, can have the same effect (Swann et al., 1987). Severity of manic symptoms has been found to correlate with noradrenaline metabolite concentrations in cerebrospinal fluid (Swann et al., 1987) and various laboratory measures of impulsivity (Swann et al., 2001). Stimulation of noradrenaline release by the nonselective
