, 2012). This pattern of increased prefrontal activity is often coupled with decreased activity in the amygdala during the reappraisal of aversive or threatening stimuli (Delgado et al., 2008 and Ochsner et al., 2002). Collectively, this work has led to a provisional model of cognitive emotion regulation in which the dlPFC—consistent with its broader role in executive function—facilitates the online maintenance and manipulation of information needed for reappraisal to take place, while activity in the amygdala Selleckchem Cabozantinib diminishes as the emotional significance of regulated stimuli dampen. The inhibitory nature of this PFC-amygdala relationship

is thought to be mediated by the vmPFC (Delgado et al., 2008 and Ochsner et al., 2012) suggesting a mechanism through which dlPFC activity could modulate amygdala activity during cognitive regulation (Hartley and Phelps, 2009, Ochsner and Gross, 2007 and Schiller and Delgado, AC220 molecular weight 2010). Cognitive emotion regulation relies on a number of higher-level executive functions including intact working memory,

used to maintain representations of relevant information during emotion regulation; response inhibition, which can facilitate the inhibition of automatic responses to threatening cues; and cognitive flexibility, which enables one to adopt different strategies to foster more adaptive responses (Hofmann Electron transport chain et al., 2012). However, emerging work across species suggests that these processes—and the prefrontal brain regions on which they depend—are highly sensitive to the detrimental effects of acute stress. Specifically, these impairments are thought to arise from excessive levels of stress hormones, which have been shown in animals to disrupt neuronal activity (i.e., alter firing rates) and lead to a broad range of cognitive impairments (Arnsten and Goldman-Rakic, 1998, Arnsten, 2009 and Murphy et al., 1996). The PFC relies on a delicate balance of catecholamines such as noradrenaline and dopamine, which each exert an inverted U-shaped influence on lateral

PFC physiology and function in which optimal levels facilitate neuronal firing patters and PFC-dependent task performance, while supraoptimal levels—such as those that may be reached during or after stress exposure—lead to impairments. Research in humans is consistent with this: brief exposure to stress has been shown to impair executive functions including working memory capacity (Duncko et al., 2009, Elzinga and Roelofs, 2005, Luethi et al., 2009, Roozendaal et al., 2004 and Schoofs et al., 2009), cognitive flexibility (Alexander et al., 2007 and Plessow et al., 2011), and goal-directed behavior (Otto et al., 2013), and leads to metabolic reduction in areas selective to emotion regulation, including the vmPFC (Kern et al., 2008) and the dlPFC (Qin et al., 2009).