Altered posterior mid-cingulate cortex activation during adaptive coding in individuals with schizotypal traits, subthreshold depression and autistic traits.

Anhedonia is a shared symptom for schizophrenia, major depressive disorder and autism spectrum disorder. Adaptive coding concerns the rescaling of the neural output to the range of values expected in the current context, and impaired adaptive coding may contribute to anhedonia. Previous research seldom compared the neural correlates of adaptive coding between individuals with schizotypal trait (ST), subthreshold depression (SD), autistic trait (AT). Thirty-five ST, 35 SD, 23 AT and 34 HC completed the adaptive version of the Monetary Incentive Delay Task in fMRI. Adaptive coding performance for the expected value (EV) and outcome value (OV) was recorded. Another separate task was used to measure the adaptive coding performance behaviourally. Anhedonia was measured using self-reported questionnaires. ST, SD and AT groups showed hyper-activation of the posterior mid-cingulate cortex (pMCC) during EV adaptation of reward as compared to HC. SD showed hyper-activation in supplementary motor area (SMA) as compared to HC during OV adaptation to rewards. The neural and behavioural performance of adaptive coding were correlated with self-reported pleasure experience in ST, SD and AT groups. These findings suggested shared and distinct aberrant neural patterns of adaptive coding in individuals with ST, SD and AT. The atypical adaptive coding performance was linked to anhedonia in all subclinical groups. Adaptive coding may have an important role in intervention or prevention of anhedonia symptoms.