Ventral striatal and medial prefrontal BOLD activation is correlated with reward-related electrocortical activity: A combined ERP and fMRI study

Models of reinforcement learning represent reward and punishment in terms of reward prediction errors (RPEs), quantitative signed terms describing the degree to which outcomes are better than expected (positive RPEs) or worse (negative RPEs). An electrophysiological component known as feedback related negativity (FRN) occurs at frontocentral sites 240-340 ms after feedback on whether a reward or punishment is obtained, and has been claimed to neurally encode an RPE. An outstanding question however, is whether the FRN is sensitive to the size of both positive RPEs and negative RPEs. Previous attempts to answer this question have examined the simple effects of RPE size for positive RPEs and negative RPEs separately. However, this methodology can be compromised by overlap from components coding for unsigned prediction error size, or "salience", which are sensitive to the absolute size of a prediction error but not its valence. In our study, positive and negative RPEs were parametrically modulated using both reward likelihood and magnitude, with principal components analysis used to separate out overlying components. This revealed a single RPE encoding component responsive to the size of positive RPEs, peaking at ~330 ms, and occupying the delta frequency band. Other components responsive to unsigned prediction error size were shown, but no component sensitive to negative RPE size was found.

Social comparison is ubiquitous across human societies with dramatic influence on people's well-being and decision making. Downward comparison (comparing to worse-off others) and upward comparison (comparing to better-off others) constitute two types of social comparisons that produce different neuropsychological consequences. Based on studies exploring neural signatures associated with downward and upward comparisons, the current study utilized a coordinate-based meta-analysis to provide a refinement of understanding about the underlying neural architecture of social comparison. We identified consistent involvement of the ventral striatum and ventromedial prefrontal cortex in downward comparison and consistent involvement of the anterior insula and dorsal anterior cingulate cortex in upward comparison. These findings fit well with the "common-currency" hypothesis that neural representations of social gain or loss resemble those for non-social reward or loss processing. Accordingly, we discussed our findings in the framework of general reinforcement learning (RL) hypothesis, arguing how social gain/loss induced by social comparisons could be encoded by the brain as a domain-general signal (i.e., prediction errors) serving to adjust people's decisions in social settings. Although the RL account may serve as a heuristic framework for the future research, other plausible accounts on the neuropsychological mechanism of social comparison were also acknowledged. Hum Brain Mapp 39:440-458, 2018.V C 2017 Wiley Periodicals, Inc.

Normal maintenance of human motivation depends on the integrity of subcortical structures that link the prefrontal cortex with the limbic system. Structural and functional disruption of diff erent networks within these circuits alters the maintenance of spontaneous mental activity and the capacity of aff ected individuals to associate emotions with complex stimuli. The clinical manifestations of these changes include a continuum of abnormalities in goal-oriented behaviours known as apathy. Apathy is highly prevalent in Parkinson's disease (and across many neurodegenerative disorders) and can severely aff ect the quality of life of both patients and caregivers. Diff erentiation of apathy from depression, and discrimination of its cognitive, emotional, and auto-activation components could guide an individualised approach to the treatment of symptoms. The opportunity to manipulate dopaminergic treatment in Parkinson's disease allows researchers to study a continuous range of motivational states, from apathy to impulse control disorders. Parkinson's disease can thus be viewed as a model that provides insight into the neural substrates of apathy.