Abstract
Contrasting theories of schizophrenia propose that the disorder is characterized by a deficit in phasic changes in dopamine activity in response to ongoing events or, alternatively, by a weakness in the representation of the value of responses. Schizophrenia patients have reliably reduced brain activity following incorrect responses but other research suggests that they may have intact feedback-related potentials, indicating that the impairment may be specifically response-related. We used event-related brain potentials and computational modeling to examine this issue by comparing the neural response to outcomes with the neural response to behaviors that predict outcomes in patients with schizophrenia and psychiatrically healthy comparison subjects. We recorded feedback-related activity in a passive gambling task and a time estimation task and error-related activity in a flanker task. Patients’ brain activity following an erroneous response was reduced compared to comparison subjects but feedback-related activity did not differ between groups. To test hypotheses about the possible causes of this pattern of results, we used computational modeling of the electrophysiological data to simulate the effects of an overall reduction in patients’ sensitivity to feedback, selective insensitivity to positive or negative feedback, reduced learning rate, and a decreased representation of the value of the response given the stimulus on each trial. The results of the computational modeling suggest that schizophrenia patients exhibit weakened representation of response values, possibly due to failure of the basal ganglia to strongly associate stimuli with appropriate response alternatives.
Highlights
For more than 30 years, pharmacological, neurophysiological, and neuroimaging studies have documented that the dopamine (DA) system is disrupted in schizophrenia
Consistent with the hypothesis that the feedback ERN is relatively intact in schizophrenia, there was no difference between groups in feedback ERN difference wave amplitude, F (1, 51) = 0.10, p = 0.75, η2p = 0.002
Recent empirical and theoretical advances in our understanding about the role of phasic dopamine in schizophrenia have informed contrasting models of the illness which focus on disruption of the reward prediction error signals (RPEs) signal (Corlett et al, 2007; Frank, 2008; Fletcher and Frith, 2009) and impairment in the representation of response value (Gold et al, 2008)
Summary
For more than 30 years, pharmacological, neurophysiological, and neuroimaging studies have documented that the dopamine (DA) system is disrupted in schizophrenia (see Davis et al, 1991 for a review). The antipsychotic effects of DA-blocking medications provide evidence of a relationship between tonic DA levels and the symptoms of schizophrenia but recent theoretical and empirical advances in the study of phasic DA activity (Schultz, 1998, 2002) allow new understanding of some of the most persistent cognitive and motivational deficits characteristic of the illness (Ziauddeen and Murray, 2010) Many of these advances are based upon findings from studies of transient changes in mesencephalic DA neurons in primates (Schultz, 1998, 2002). RPE signals are based on neural representations of value associated with different response alternatives (Montague and Sejnowski, 1994; Niv, 2009) and these values appear to be represented in the basal ganglia (Samejima et al, 2005; Lau and Glimcher, 2008) where the critic is thought to reside (O’Doherty et al, 2004)
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