Similarly, Womelsdorf and colleagues (2010) have shown that local field potentials (LFPs) in the theta band observed within macaque dACC could discriminate which of two stimulus-response mapping rules (pro- versus anti-saccade) would be used prior to appearance of the stimulus. Furthermore, this rule selectivity was absent prior to error trials, consistent with

the hypothesis that activity in dACC was required to specify the identity of the task-appropriate control signal. Interestingly, when rule-selective activity reemerged prior to a correct trial following an error, the selectivity was seen earlier than on correct trials that followed a previous correct one (see find more also Johnston et al., 2007). A subsequent study from this group used a similar task to provide causal support for this control specification role ( Phillips et al.,

2011). They found that stimulating dACC during the response preparation period significantly facilitated antisaccade performance (accelerating responses without increasing error rate), but had a less consistent influence on prosaccade performance, a complement to the impairments (slowing) previously found in human dACC lesion patients performing an antisaccade task ( Gaymard et al., 1998). Additional evidence consistent with identity specification comes from one of the most comprehensive analyses to date of human patients with focal brain lesions (Gläscher SP600125 manufacturer et al., 2012). This study combined data from four different set-shifting tasks into a single “cognitive control factor” and found that the poorest performance along this factor was associated with lesions in rostral dACC. These findings are consistent with a causal role for dACC in specifying control identities. It is also consistent with its role in specifying the intensity of those control signals. Motivation. A role in specifying control intensity is consistent with the earliest observations regarding dACC function,

which ascribed to it a function in “motivation,” driven in part by the observation that medial frontal damage can lead to gross deficits in motivated behavior (e.g., abulia; see Holroyd and Yeung, 2012). More recent proposals have suggested that dACC motivates these or ‘energizes’ action or task engagement based on current incentives ( Holroyd and Yeung, 2012, Kouneiher et al., 2009 and Stuss and Alexander, 2007). In support of this, circumscribed lesions that encompass dACC produce longer overall reaction times (e.g., Alexander et al., 2007 and Fellows and Farah, 2005), and higher false alarm rates (e.g., Løvstad et al., 2012 and Tsuchida and Fellows, 2009). These are consistent with a role for dACC in specifying control intensity. Adaptive Adjustments in Control Intensity.