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Rostral and dorsal anterior cingulate cortex make dissociable contributions during antisaccade error commission - PubMed

  • ️Sat Jan 01 2005

Rostral and dorsal anterior cingulate cortex make dissociable contributions during antisaccade error commission

Frida E Polli et al. Proc Natl Acad Sci U S A. 2005.

Abstract

The anterior cingulate cortex (ACC) participates in both performance optimization and evaluation, with dissociable contributions from dorsal (dACC) and rostral (rACC) regions. Deactivation in rACC and other default-mode regions is important for performance optimization, whereas increased rACC and dACC activation contributes to performance evaluation. Errors activate both rACC and dACC. We propose that this activation reflects differential error-related involvement of rACC and dACC during both performance optimization and evaluation, and that these two processes can be distinguished by the timing of their occurrence within a trial. We compared correct and error antisaccade trials. We expected errors to correlate with an early failure of rACC deactivation and increased activation of both rACC and dACC later in the trial. Eighteen healthy subjects performed a series of prosaccade and antisaccade trials during event-related functional MRI. We estimated the hemodynamic responses for error and correct antisaccades using a finite impulse-response model. We examined ACC activity by comparing error and correct antisaccades with a fixation baseline and error to correct antisaccades directly. Compared with correct antisaccades, errors were characterized by an early bilateral failure of deactivation of rACC and other default-mode regions. This difference was significant in rACC. Errors also were associated with increased activity in both rACC and dACC later in the trial. These results show that accurate performance involves deactivation of the rACC and other default mode regions and suggest that both rACC and dACC contribute to the evaluation of error responses.

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Figures

Fig. 1.
Fig. 1.

Schematic depiction of a 4,000-ms saccadic trial. Trials began with a 300-ms cue instructing participants to make either a PS or an AS. The cue was then replaced by a fixation ring, which shifted to one of two target locations flanking the cue horizontally. This target was the one to which subjects responded. The ring remained in the peripheral location for 1,000 ms, then returned to the center for 1,000 ms.

Fig. 2.
Fig. 2.

Findings of differential rACC and dACC activity at early and later time points during correct and error antisaccade trials. Statistical activity maps displayed on the inflated medial cortical surfaces for the three contrasts (correct ASs vs. fixation, error ASs vs. fixation, and error vs. correct ASs) for the two early time points, 2and 4s(a), and the two later time points, 6 and 8 s (b). Gray masks cover noncortical regions in which any activation is displaced. (c) The HDRs for the dACC and rACC, as well as posterior cingulate cortex (PCC), dorsomedial PFC (DMC), superior temporal cortex (STC), and angular gyrus (AG) minima in the correct vs. fixation contrast. (d) The HDRs for the dACC and rACC maxima in the error vs. correct contrast. Time in seconds is on the x axis, and percent signal change relative to the fixation baseline is on the y axis. All HDRs are an average of left- and right-hemisphere minima/maxima HDRs. Although clusters <120 mm2 are displayed, they are not considered significant.

Fig. 3.
Fig. 3.

Statistical map for vertex-wise cortical surface linear regression of number of errors by raw estimates of the hemodynamic activity (BOLD, blood oxygen level-dependent) at 4 s in the correct ASs vs. fixation contrast displayed on the inflated right medial surface.

Fig. 4.
Fig. 4.

Statistical maps displayed on the inflated medial and lateral cortical surfaces for the correct AS vs. PS trials at 4 s.

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