Figure 4.
Neurophysiological responses to reversals in caudate, insula, and thalamus. (A) Contrast of BOLD activation in a reversal trial (Treversal, unexpected outcome) minus the trial before reversal (Treversal − 1, fully expected outcome), averaged over all conditions (placebo/l-dopa and salient/null). Differential activation is seen in bilateral insula, thalamus, and caudate [peak (x, y, z) MNI coordinates (z scores)—insula: −27, 17, 7 (4.43) and 42, 20, 1 (5.12); thalamus: −6, −19, 7 (4.74) and 6, −22, 7 (4.08); caudate: 12, 5, 7 (4.37); P < 0.005 FWE-corrected]. (B–D) Plots of mean parameter estimates (β values) for the reversal trial and the trial before reversal in the insula (B), thalamus (C), and caudate (D), contingent upon subsequent successful reversal shifting (i.e., a behaviorally validated response). Here, we observed a prediction error-type response (reduced activation at the time an unexpected/surprising outcome was presented) across trial types [salient loss trials on left; neutral/null trials on right; placebo (gray bars), l-dopa (white bars)]. (Treversal − 1− Treversal) contrast effects per condition: bilateral insula – (salient loss)placebo: t(1,14) = −5.93, P < 0.001, (null)placebo: t(1,14) = −3.41, P = 0.004; (salient loss)l-dopa: t(1,14) = −2.86, P = 0.012; (null)l-dopa: t(1,14) = −5.03, P < 0.001. Bilateral thalamus—(salient loss)placebo: t(1,14) = −4.65, P < 0.001, (null)placebo: t(1,14) = −3.14, P = 0.007; (salient loss)l-dopa: t(1,14) = −1.9, P = 0.07; (null)l-dopa: t(1,14) = −3.11, P = 0.008. Left caudate—(null)placebo: t(1,14) = −1.807, P = 0.092; (salient loss)l-dopa: t(1,14) = −2.803, P = 0.014. Within-subject standard error bars are shown. *P < 0.05; +P < 0.1.