Conflict in cingulate cortex function between humans and macaque monkeys: More apparent than real.

these and other alternative hypotheses using human subjects. The relative merits of these alternative hypotheses are not the focus of this commentary. Over the last decade this literature derived from human studies has been supplemented by neurophysiological data from macaque monkeys. In monkeys performing an eye movement stop signal task, neurons are found in the supplementary eye field that signal when errors are produced, when reward is delivered and when conflict occurs [Stuphorn et al., 2000]. In contrast, multiple neurophysiological studies of the macaque monkey ACC have reported error and reward signals but an absence of a conflict signal in tasks that should engender such response conflict [Ito et al., 2003; Nakamura et al., 2005; Emeric et al., 2008]. Cole et al. [2009] argue that the lack of a single neuron conflict signal in macaque monkeys in contrast to humans is a manifestation of a fundamental species difference and a greater sensitivity of functional brain imaging methods to weak conflict signals. We will argue that simpler alternative interpretations have not been ruled out. To account for the apparent incommensurability of results in monkeys and humans, Cole et al. [2009] emphasize speA recent review in Trends in Neuroscience by Cole, Yeung, Freiwald and Botvinick identified a potential fundamental difference in functional properties of the anterior cingulate cortex (ACC) of humans and macaque monkeys [Cole et al., 2009]. The key function in question is monitoring of conflict in response preparation. The conflict hypothesis, defended by the senior authors of the review as a general theory of ACC function, states that when a task calls for multiple competing responses, then executive control is required to resolve the conflict. It is supposed to explain the origin and purpose of event-related potential components such as the error-related negativity (ERN) that occurs after response errors [reviewed by Taylor et al., 2007] and a body of functional brain imaging data. The ERN can be generated by a dipole in the ACC; however, uncertainties in the localization of this dipole as well as other neuroimaging and lesion data demonstrate that more dorsal areas of medial frontal cortex including preSMA also contribute to performance monitoring [e.g. Garavan et al., 2003]. The ERN can also be identified with a reward prediction error originating from the dopamine system [Taylor et al., 2007]. An active literature has developed evaluating Published online: August 6, 2010