Motivational deficits (avolition and anhedonia) have historically been considered important negative
Motivational deficits (avolition and anhedonia) have historically been considered important negative symptoms of schizophrenia. we describe different aspects of the concept of expected value (EV) such as the distinction between the EV of stimuli and the expected value of actions the acquisition Fisetin (Fustel) of value vs. the estimation of value and the discounting of value as a consequence of time or effort required. We conclude that avolition and anhedonia in SZ are most commonly tied to aberrant signals for expected value in the context of learning. We discuss implications for further research on the neural substrates of motivational impairments in psychiatric illness. of pleasure (“consummatory hedonics”; Cohen and Minor 2008 Gard et al. 2007 Partially based on this evidence we (Gold et al. 2008 hypothesized that avolition results from a failure to look forward to pleasurable outcomes (“anticipatory hedonics”) by virtue of the assignment of incentive salience to cues. As defined by Berridge and Robinson (1998) a stimulus becomes imbued with incentive salience when it is transformed from a neutral object into an object of attraction that animals will work to acquire. This is the essential outcome of reinforcement learning (RL) and it is thought to be a primary functional role of dopamine in the nervous system (Berridge and Robinson 1998 The updating of the incentive value of a stimulus is thought to occur via the signaling of reward prediction errors (RPEs) which are mismatches between expected and obtained outcomes. Thus a to update the incentive value of a stimulus could happen for at least three reasons: 1) the signal of the expected outcome is degraded or inaccurate; 2) the signal of the obtained outcome is degraded or inaccurate; or 3) the mechanism for computing the RPE is dysfunctional. Given the evidence that signals related to reward receipt in schizophrenia are intact (Cohen and Minor 2010 considerable attention has been focused on the other two possibilities: that the signal of the expected outcome is degraded or inaccurate and that the mechanism for computing the RPE is dysfunctional. In fact there is considerable evidence that acutely-ill patients (particularly those that are unmedicated) have genuinely-disrupted RPE signaling (Murray et al. 2007 Schlagenhauf et al. 2014 Schlagenhauf et al. 2009 with important implications for RL and belief-formation. Furthermore there have been numerous findings of correlations between measures of both positive symptoms in schizophrenia and supposed RPE signals in the brain (Gradin et al. 2011 It is however much less certain that RPE signaling is abnormal in chronic medicated Fisetin (Fustel) patients (Walter et al. 2009 Waltz et al. 2010 despite clear evidence of reinforcement learning deficits in these patients (Farkas et al. 2008 Waltz et al. 2007 Furthermore measures of RL performance have been shown to correlate with the severity of motivational deficits in chronic SZ patients. Were RL deficits to persist in stably-medicated SZ patients despite evidence of intact RPE signaling it would suggest that aberrant RPE-driven learning observed in medicated SZs may be more a problem of faulty to the PE computation than dysfunction in the mechanism itself. In this chapter our purpose is to evaluate the data arguing for and against the idea that the signaling of expected value (EV) in chronic SZ patients Fisetin (Fustel) relates to motivational deficits which are thought to persist Rabbit Polyclonal to NFIL3. throughout the illness and be largely unaffected by antipsychotic medications. This area has been the focus of numerous basic and clinical studies. Prior to discussing clinical findings we will first review the basic concepts and methods that have served to guide the field. 2 Identifying a relationship between EV and avolition: Considerations 2.1 How do we quantify the severity of motivational deficits in schizophrenia? The first step in linking an aspect of behavioral performance or a purported neural signal to the severity of motivational deficits in Fisetin (Fustel) a psychiatric population is to establish how one quantifies the severity of motivational deficits. In the field of schizophrenia research motivational deficits are commonly thought.