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Negative symptoms are core features of schizophrenia; however, the cognitive and neural basis for individual negative symptom domains remains unclear. Converging evidence suggests a role for striatal and prefrontal dopamine in reward learning and the exploration of actions that might produce outcomes that are better than the status quo. The current study examines whether deficits in reinforcement learning and uncertainty-driven exploration predict specific negative symptoms domains.
We administered a temporal decision making task, which required trial-by-trial adjustment of reaction time (RT) to maximize reward receipt, to 51 patients with schizophrenia and 39 age-matched healthy controls. Task conditions were designed such that expected value (probability * magnitude) increased (IEV), decreased (DEV), or remained constant (CEV) with increasing response times. Computational analyses were applied to estimate the degree to which trial-by-trial responses are influenced by reinforcement history.
Individuals with schizophrenia showed impaired Go learning, but intact NoGo learning relative to controls. These effects were pronounced as a function of global measures of negative symptom. Uncertainty-based exploration was substantially reduced in individuals with schizophrenia, and selectively correlated with clinical ratings of anhedonia.
Schizophrenia patients, particularly those with high negative symptoms, failed to speed RT's to increase positive outcomes and showed reduced tendency to explore when alternative actions could lead to better outcomes than the status quo. Results are interpreted in the context of current computational, genetic, and pharmacological data supporting the roles of striatal and prefrontal dopamine in these processes.
Dopaminergic (DA) signaling plays a key role in the detection, evaluation, and prediction of rewards. Several structures that receive DA input are differentially involved in specific aspects of reward learning. For example, the striatum and orbitofrontal cortex (OFC) have been found to be involved in reward prediction and reward based decision making, with the OFC being particularly responsive to reward magnitudes (1–6). In reinforcement learning models of corticostriatal circuitry (7, 8), phasic DA signals are proposed to modify synaptic plasticity in the corticostriatal pathway (9, 10), and subsequently reinforce “Go” (learning to pursue actions that have high reward probability) and “NoGo” learning (learning to avoid actions with low reward probabilities) (7, 11). Specifically, increases in phasic striatal DA support Go learning from positive feedback via D1 receptor stimulation, whereas decreases in phasic striatal DA support avoidance learning from negative feedback via D2 receptor disinhibition.
This model has been applied to understand patterns of reward learning in Parkinson’s Disease (PD) patients (7), who have depleted striatal DA levels as a result of the disease, but increased striatal DA levels following DA medication (12, 13). Supporting the models, it has been found that PD patients on medication learn better from positive than negative decision outcomes, but patients off medication showed the opposite bias (8, 14–16). Imaging studies show that these biases are accompanied by medication-induced increased sensitivity to positive prediction errors and reduced sensitivity to negative prediction errors in the ventral and dorsolateral striatum (17). Behaviorally, these medication-induced effects have been primarily observed in tasks where participants learned stimulus-response relationships as a function of reinforcement (e.g., probabilistic learning).
Recent studies have found that SZ patients exhibit reinforcement learning abnormalities, specifically in learning to integrate the history of probabilistic positive decisions across trials (18–20). These deficits have been attributed to deficient phasic striatal dopaminergic signals and D1 receptor functionality, leading to poor Go learning. A deficit in learning to repeat those actions most likely to yield positive reinforcement may provide an intuitively appealing account that could explain negative symptoms. Several studies show that negative symptoms are associated with impairments in rapid, trial-to-trial behavioral adaptation in response to recent changes in reinforcement values, particularly during early phases of learning. We have argued that this deficit in rapid acquisition associated with negative symptoms is likely to stem from prefrontal cortical dysfunction (19, 20). Similar patterns of early learning deficits are seen in patients with orbitofrontal damage (21) and in healthy participants with the val/val genotype of the COMT gene (15), who have reduced prefrontal (and particularly, orbitofrontal) dopamine levels(22). However, relationships have also been reported between negative symptoms and deficient reward-related BOLD activity in basal ganglia structures. These changes in basal ganglia (BG) BOLD signal do not themselves necessarily indicate that the BG are the source of the deficits. For example, reduced top-down input from OFC to BG during reward would result in reduced BG activations. Thus, the neural underpinnings of reinforcement learning deficits and negative symptoms are at present unclear.
In the current study, we examined reinforcement learning in schizophrenia using a task that required subjects to modulate the response time of a single motor response, where both reinforcement probabilities and magnitudes varied as a function of RT (27). Behavioral task conditions were designed to assess Go learning, NoGo learning, and relative sensitivity to reward frequency vs. magnitude.
Computational modeling was performed in an effort to obtain a richer understanding of the behavioral findings.The modeling approach allows us to assess the degree to which participants adjust response times as a function of positive and negative prediction errors across all four of the task conditions (not solely in the conditions where it is most advantageous to do so), while distinguishing these measures from several other components to RT adjustment in the task (captured by other model parameters).
Based upon theories suggesting that SZ is associated with abnormal dopaminergic signaling (high tonic DA but low phasic DA) and impaired D1 function in particular (28–30), we hypothesized that SZ patients would fail to show relative speeding when rewards are most available for fast responses, and thus earlier responding results in better-than-expected outcomes (i.e.,positive prediction errors). Conversely, based on our previous findings (19) and the fact that patients were medicated with D2 antagonists, we hypothesized that SZ patients would show intact slowing as a function of negative prediction errors when early responses produced outcomes that were lower than expected on average. The latter interpretation is supported by computational simulations showing that D2 blockade enhances NoGo learning and RT slowing (see (31)) and recent demonstration that D2 blockade enhances NoGo learning in Tourette's syndrome patients (16).
Evidence for such a pattern of spared sensitivity to negative outcomes, coupled with reduced ability to learn to approach responses leading to positive reinforcement could be considered a perfect neurobehavioral recipe for avolition and anhedonia. In light of previous studies indicating that reinforcement learning impairments are most severe in high negative symptom patients (32, 33), we therefore also examined the role of negative symptoms in Go and NoGo learning, with the prediction that high negative symptom patients would show the greatest Go learning impairment and comparatively intact NoGo performance Alternatively, rather than resulting from reinforcement learning deficits per se, some aspects of negative symptoms may be characterized by a reduced tendency to appropriately explore alternative actions in the hope that they might produce better outcomes. Notably, the computations of outcome uncertainty used to guide exploration are thought to depend on neuromodulation within the prefrontal cortex (PFC) (34–36). Accordingly, a recent genetic study with the same task used here showed that, consistent with striatal DA genetic effects on Go/NoGo learning, individual differences in uncertainty-driven exploration were predicted by COMT val/met genotype (36). We thus applied the same computational analyses of trial-by-trial responses in the current study to investigate the prediction that patients would show not only differences in speeding and slowing as a function of prediction errors, but also whether they would exhibit uncertainty-driven exploration.
Participants included 51 patients meeting DSM-IV-TR criteria for schizophrenia and 39 healthy controls (CN). The patients were recruited from the outpatient clinics at the Maryland Psychiatric Research Center and were studied during a period of clinical stability. All patients met DSM-IV diagnostic criteria for schizophrenia or schizoaffective disorder. Consensus diagnosis was established with a best-estimate approach based on medical records and confirmed using the Structured Clinical Interview for DSM-IV (SCID) (37). All patients were receiving antipsychotic medications.
Control subjects were recruited through random digit dialing and word of mouth among individuals recruited through random digit dialing. All controls underwent a screening interview and denied lifetime and family history of psychosis and any active Axis I disorder on the SCID. All participants denied lifetime history of significant neurological conditions and recent substance abuse as determined by the SCID (none within 6 months). Upon entry to our subject pool, we routinely screen for substance use via urine toxicology testing. In the current study, targeted urine toxicology testing was performed in instances where there were suspicions of substance use. Patient and control groups did not significantly differ in age, parental education, gender, or ethnicity. Patients had fewer years of total education and lower WASI estimated full-scale IQ’s than controls (see Table 1).
Schizophrenia patients were also divided into High (HI-NEG) and Low Negative (LOW-NEG) symptom groups based upon a median split on the Scale for the Assessment of Negative Symptoms (SANS: (38, 39)) total score. The 22 item version of the SANS developed in the CONSIST clinical trial was used (39), which has fewer items than the original 30- or 25-item version, with total scores ranging from 0–110. The three groups did not significantly differ on age, parental education, gender, or ethnicity; however, they did differ on IQ, such that CN had significantly higher IQ than both schizophrenia groups. There were no differences in IQ between the HI-NEG and LOW-NEG patients. HI-NEG and LOW-NEG patients significantly differed on the BPRS negative symptom factor score, but not on positive symptoms, disorganization, or total scale score. HI-NEG and LOW-NEG patients were also prescribed a similar regimen of antipsychotic medications at the time of testing and did not differ on chlorpromazine (CPZ) equivalent dosage (40) (see Table 1).
The current tests were administered as part of a larger battery of reward-learning, symptom interview, and neuropsychological measures. For each subject, demographic, diagnostic, and symptom ratings were completed prior to administration of the neurocognitive evaluations. Symptom interviews included the SANS and Brief Psychiatric Rating Scale (BPRS: (41)). Patient and control participants recruited from the community received monetary compensation for participation. Study personnel administering the neurocognitive tasks included B.A. and M.A. level research assistants.
Participants completed the “temporal utility integration task” designed by Moustafa et al. (27). In this task, subjects were presented a clock face, which had a single arm that made a full turn over the course of 5 seconds. Participants were asked to press a button on a response pad at some point before the arm made a full turn. Following each response, participants were informed whether they had won points, and if so, how many. The trial ended once the subject responded using the game pad or if the 5 s duration elapsed and the subject did not respond. The inter-trial-interval (ITI) was set at 1 s. Participants completed four separate conditions, each consisting of 50 trials, in which reward probability and magnitude varied as a function of time elapsed on the clock until response. In the three primary conditions (DEV, CEV, and IEV), the number of points (reward magnitude) increased, whereas the probability of receiving the reward decreased, over time within each trial. Feedback was presented on the screen in the format of “You win XX points!” Functions within each condition were designed such that the expected value (probability*magnitude) either decreased (DEV), increased (IEV), or remained constant (CEV), across the 5 s trial duration (Figure 1). Thus in the IEV condition, early responses yielded a small number of points (lower than expected on average), and the associated negative prediction errors should lead to NoGo learning and slowed responses. In contrast, early responses in the DEV condition yielded a higher number of points than expected, and should therefore lead to Go learning/speeding. Slower responses in the IEV condition yielded more points on average, whereas in the DEV condition faster responses yielded more points.
In addition to these primary conditions, we also included a condition where expected value remains constant (like CEV), but reward probability increases and magnitude decreases as time elapses on the clock (i.e., the opposite to CEV). Since both CEV and CEVR have equal expected values across the entire clock face, any difference in response time in these two conditions can be attributed to a participants’ potential bias to learn more about reward probability than about magnitude or vice-versa. Specifically, if a subject waits longer to respond in CEVR than in CEV, it can be inferred that the participant is risk averse as they value higher probabilities of reward more than higher magnitudes of reward.
Order of condition (CEV, DEV, IEV, CEVR) was counterbalanced across participants, and a rest break was given between each of the conditions (i.e., after every 50 trials). At the beginning of each condition, subjects were instructed to respond at different times in order to find the interval on the clock that would allow them to win the most points; however, they were not told about the different rules for each condition (e.g., IEV, DEV). Each condition also had a different color clock face to highlight the uniqueness of each context, and the assignment of color was counterbalanced across conditions. The task was presented using E-Prime software.
Computational modeling was used as a tool to more specifically probe aspects of behavior in this task (36). The model allows us to estimate the degree to which individuals adjust their response times as a function of accumulated reward prediction errors, and uncertainty-driven exploration, distinctly from other components (see Table 2 for description of model parameters and Supplement 1 and ref. 36 for mathematical details). The major parameters of interest for the current study are αG, αN, and ε. The αG and αN parameters were used to test whether patients have deficits in learning from gains vs. losses more fully than what can be surmised from the behavioral data as the model estimates on average the degree to which subjects speed up or slow down and use positive and negative prediction errors across all conditions. The ε parameter was used to test the possibility that individuals with SZ have a reduced tendency to appropriately explore alternative actions in the hope that they might produce better outcomes.
Behavioral analyses examined RT for each condition, either for the entire block or the difference score between the second and first half of trials in each condition as indicated in the text. Repeated measures ANOVAs, one-way ANOVAs, t-tests, and chi-square analyses were calculated to determine group differences. Spearman correlations were calculated to examine relationships between test data and symptoms. The Greenhouse-Geisser correction was applied in instances when the assumptions of sphericity or covariance were violated. Scheffe contrasts were additionally performed as post hoc tests. Wilcoxon Mann-Whitney tests were used to examine group differences on modeling parameters. Initial analyses examined between-group differences in patients and controls. However, given that SANS scores are typically bimodally distributed, we examined the role of negative symptoms using between-group analyses (i.e., comparing high negative symptom, low negative symptom, and control groups), but also reported correlations for completeness. Data were analyzed using SPSS version 12 software.
Analysis of behavioral data indicated that in both SZ patients and healthy controls, RTs in the IEV condition (No Go learning) were significantly slower than the DEV condition (Go Learning) (CN: t = −4.48, p < 0.001; SZ: t = − 4.99, p < .001), suggesting that both groups learn to adapt RTs in the expected direction (see Table S1 in Supplement 1). However, these overall means calculated across the entire block of trials mask differences in learning from the beginning to the end of the condition. As such, difference scores were computed separately for each condition to estimate RT adaptation from the first half of trials to the second half of trials (2nd half of trials – 1st half of trials). Consistent with hypotheses, SZ patients fail to learn to speed up by the end of the block in the DEV (Go learning) condition as much as CN, but perform similarly to CN in the IEV (No Go) and CEV (Control) conditions (see Figure 2). This was confirmed statistically by separate repeated measures ANOVAs, which indicated that groups significantly differed on the DEV condition, F (1, 88) = 9.49, p = 0.003 (η2=.10), but not the IEV, F (1, 88) = 0.01, p = 0.913 (η2=.00), or CEV conditions, F (1, 88) = 1.86, p = 0.176 (η2=.02). These behavioral findings are consistent with intact No Go, but impaired Go learning in schizophrenia1.
Computational modeling was used to obtain a richer understanding of these behavioral findings on Go and No Go learning. Overall, the computational model encompassing the specified combination of parameters (see Supplemental Results in Supplement 1) and which was the best fit to the data in our previous study, also provided a reasonable fit to the behavioral data here (Figure 3).
Significant parameter differences between SZ patients and controls were observed for ε, the degree to which exploration occurs in proportion to relative uncertainty about reward outcomes, F (1,88) = 9.1, p = .003. These differences remain significant after bonferroni correction (Figure 4). Additional analyses also confirmed that the exploration effect in schizophrenia was specific to uncertainty, as groups did not differ in measures of overall RT variability or RT swings (see Figure S4 in Supplement 1).There was also a trend for αG to be smaller in patients (Wilcoxon Mann-Whitney test, two-tailed p = 0.07), consistent with the behavioral results, whereby patients exhibited deficits in learning to speed responses in the DEV condition. A follow-up logistic regression with both parameters entered as predictors confirmed that both the explore (p <.02) and αG parameters (p=.028) were independently predictive of SZ. There were no other significant differences between patients and controls in any of the other parameters (see Table 3).
A regression analysis shed further light onto this interpretation, revealing that individual differences in the tendency to speed up to maximize rewards in the DEV condition is predicted by αG (p = .018), such that higher parameters were associated with increased speeding. No such difference was seen in terms of the model parameter estimating the degree to which participants slow down as a function of negative prediction errors.
We also conducted analyses examining behavioral and modeling parameters in patients with High Negative Symptoms (HI-NEG), Low Negative Symptoms (LOW-NEG), and Controls (CN). As can be seen in Figure 5, the HI-NEG group showed significantly reduced speeding from the first to second half of trials in the DEV condition, consistent with a Go learning deficit in high negative symptom patients. One-way ANOVAs, conducted with difference scores (2nd half of trials – 1st half of trials) as the dependent variable supports this interpretation, indicating that the 3 groups significantly differed on DEV, F (2, 85) = 4.78, p=0.01 (η2=.11), but not IEV, F (2, 85) = 0.23, p = 0.37 (η2=.01), or CEV, F (2, 85) = 0.99, p = 0.73 (η2=.02). Post hoc Scheffe contrasts conducted for the DEV change condition were significant between the HI-NEG and CN (p = .02), but not the LOW-NEG and CN (p = .14) or HI-NEG and LOW-NEG (p = .68) groups. The correlation between the SANS total score and DEV and IEV conditions was nonsignificant. The discrepancy between the significant between-subjects analysis on the DEV condition and nonsignificant correlation between negative symptoms and DEV learning is likely explained by the fact that Go learning deficits were most pronounced in HI-NEG patients, but still present in LOW-NEG patients as well, thereby attenuating the strength of the correlation.
In a separate analysis of behavioral data, HI-NEG patients also failed to show either a probability or magnitude bias, whereas CN and LOW-NEG both showed a bias to learn more about probability than magnitude (see Figure S1 in Supplement 1 for discussion).
One-way ANOVAs indicated that the 3 groups failed to significantly differ on any parameter other than exploration, F (2, 85) = 5.02, p = 0.009 (HI-NEG: M = 1187, SD = 1561; LOW-NEG: M = 1323, SD = 1678). Post hoc Scheffe contrasts indicated significant differences between HI-NEG and CN (p = 0.03) subjects; however, LOW-NEG and CN (p = 0.06) and HI-NEG and LOW-NEG (p = 0.97) did not significantly differ. Interestingly, correlational analyses indicated that the dramatic reduction in exploration was most severe in patients with high avolition-anhedonia SANS summary scores (r = −0.28, p < 0.05). There were no significant correlations between ε and the restricted affect (SANS alogia + blunted affect items) summary score (r = 0.05) or the SANS total, suggesting that the relationship may be specific to the avolition-anhedonia domain. Follow-up correlational analyses using the avolition and anhedonia global scores indicated that the relationship with exploration was specific to anhedonia (Anhedonia r = −0.44, p < 0.01; Avolition r = −0.15, p >0.3) (see Figure 6). The test for significant differences between these correlations approached significance (z = −1.54, p = 0.06).
Given the unique association with anhedonia, we further investigated whether the association between anhedonia and exploration was specific to uncertainty, and determined that anhedonia was only associated with uncertainty-driven exploration, and not overall RT variability or consecutive RT variance. Furthermore, control model simulations revealed that other models of RT swings, including parameters for lose-switch, or regression to the mean, did not correlate with anhedonia (see Supplemental Results and Figure S2 in Supplement 1).
Correlational analyses indicated that CPZ dosage was not significantly correlated with behavioral performance in any of the conditions (all p’s > 0.16) or modeling parameters (all p’s > 0.14). Analyses examining between-group differences in patients categorized as a function of low and high potency D2 blockade antipsychotics indicated no differences between medication groups in behavioral task conditions (see Supplemental Results in Supplement 1).
Two main findings emerged from the current study. First, behavioral data indicated that patients were less able to learn to speed up to maximize rewards, which is consistent with a Go learning deficit. The model simulations suggest this deficit may at least in part be due to lower αG parameter, as a regression analysis revealed that individual differences in the tendency to speed up to maximize rewards in the DEV condition is predicted by αG, such that higher parameters were associated with increased speeding. Given that SZ showed a deficit in both αG and the DEV, but not αN or IEV, we feel that the results of the computational model provide further confidence that the deficits specific to Go learning in schizophrenia are reliable. Furthermore, symptom sub-group analyses revealed that, in terms of DEV performance, Go learning deficits are most severe in patients exhibiting greater severity of negative symptoms.
These findings are consistent with our previous probabilistic selection study indicating that SZ is associated with impaired Go learning and intact No Go learning (19). When viewed in conjunction with neurocomputational models of corticostriatal circuitry in reinforcement learning (7, 8), the current behavioral and modeling findings are suggestive of potential dysfunction in the direct D1 driven BG pathway leading to abnormalities in using positive feedback to guide behavior, with relatively intact function in the D2 driven, indirect pathway leading to normal use of probabilistic negative feedback in decision making. This BG-based account is supported by other evidence indicating that BG dopamine acts to speed responding toward rewarding cues (42, 43), as well as pharmacological and animal studies showing that this process likely relies on D1-driven activation and Go learning (44–46). However, this interpretation is of course speculative, and cannot be confirmed without conducting a study on unmedicated 1st episode patients to see if No Go learning improves when patients are treated with D2 blocking antipsychotics.
A second major finding was that SZ patients exhibited a large and reliable reduction in the tendency to make exploratory behavioral adjustments toward responses that could potentially yield larger expected values than those obtained by staying with the status quo. Additionally, given that there was no association between anhedonia and overall RT variability or consecutive variance, anhedonia appears to be selectively associated with the failure to initiate the proactive strategy of adjusting responses to gather more information in order to reduce uncertainty about potential benefits of alternative behaviors. These findings demonstrate the usefulness of computational modeling approaches to psychiatry (25, 47–51).
We posit that these effects are related to degradations in prefrontal cortical dopaminergic function, often attributed as a source of negative symptoms (28, 30, 52, 53). This interpretation is supported by our recently reported gene-dose effect of the val/met polymorphism of the COMT gene in healthy individuals performing this same task (36), which indicated that the val/val genotype was characterized by the lowest degree of uncertainty-driven exploration and the met/met genotype with the greatest degree of exploration. Variations in COMT affect prefrontal, and particularly orbitofrontal, dopamine levels (22), and a recent study reported a COMT gene dose effect on orbitofrontal activity during reward receipt (54). Thus together, these studies support the assertion that the val/val genotype shares features of cognitive dysfunction observed in SZ (55). Finally, ongoing imaging work in healthy individuals (56), together with other related studies (35, 57), suggest that relative uncertainty computations associated with exploration are represented in prefrontal cortical activation patterns. Finally, even if the computations of expected reward values are relatively intact in SZ, it is possible that patients with anhedonia explicitly assign a negative expected value to uncertain outcomes, due to their prior expectations (see (51) for a related model of depression). Regardless of the neural mechanism, our findings suggest that anhedonia may result from an inability to determine when to explore actions that might improve one's ability to obtain rewards.
Of particular interest was that reduced uncertainty-driven exploration correlated with the Avolition-Anhedonia domain on the SANS, but not the Restricted Affect factor. Additionally, the effect was more highly related to anhedonia than avolition. This result is potentially informative about differences in the pathology of these symptom domains. As rated by the SANS, anhedonia reflects a behavioral component of reward seeking (e.g., initiating social activities, sexual interest/and or activity, pursuing recreational activities, number of close relationships), rather than the capacity to experience pleasure, which is often inferred from behavior. Avolition items on the SANS are less related to reward seeking behavior, and more broadly related to the frequency with which patients initiate and persist in many kinds of tasks which is likely to be influenced by a number of factors, such as disorganization, generalized cognitive impairment, and sedation. The significant correlation with anhedonia, but not avolition may therefore reflect that reduced reward seeking behavior in schizophrenia is critically related to the extent to which patients make exploratory choices when they are uncertain about the value of alternative actions and whether they might produce better outcomes than the status quo.
Results should be viewed with certain limitations in mind. First, analyses regarding the role of medication on task performance should be viewed with caution, as CPZ equivalents for atypical medications may not be appropriate and D2 potency classifications provide only a gross estimate of the effects of different antipsychotics. A more definitive test of antipsychotic effects should be conducted in first episode patients tested on and off medications. Second, we did not collect DNA in this study and it is unclear whether the COMT genetic effect observed in healthy individuals on exploration may partially contribute to the effects of anhedonia and SZ reported here. Finally, although the SANS is still the gold standard negative symptom assessment in the field, it has recently been suggested that newer measures being developed in response to the NIMH MATRICS (e.g., (60)) initiative may provide a more comprehensive and current assessment of negative symptom dimensions. As such, it is unclear whether the relationship reported between SANS anhedonia and exploration may actually reflect some other component of negative symptoms on these newer scales.
In summary, the current findings have important implications for understanding the etiology of schizophrenia. Results from the computational model and behavioral data indicate that patients have deficits in Go learning, which appear to be due to reduced sensitivity to positive prediction errors. Thus patients show a reduced sensitivity to the impact of rewarding outcomes on future behavioral choices. Furthermore, patients display reduced uncertainty-driven exploration, which was specifically associated with greater severity of anhedonia. Thus, patients are less likely to explore, and therefore less likely to discover, that an alternative response might yield more rewarding outcomes. While these deficits are independent of one another in the model, at a clinical level it is easy to imagine how these impairments might amplify one another and result in a narrow behavioral repertoire and a lack of goal-directed, reward-seeking behavior.
This research was supported by US National Institutes of Mental Health grant R01 MH080066-01. We would also like to thank the subjects who participated in the study and staff at the Maryland Psychiatric Research Center who made the completion of the study possible. We are especially thankful to members of Dr. Gold’s lab, Jackie Kiwanuka, Sharon August, Lindsay Phebus, Leeka Hubzin, and Tatyana Matveeva, who conducted subject recruitment and testing. We also thank Thomas Wiecki for helpful comments on an earlier draft of this manuscript.
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1To further examine the specificity of Go and No Go learning performance in SZ and CN, we conducted a 3 condition (CEV, DEV, IEV) × 2 Time (Block 1, Block 2) × 2 Group (SZ, CN) repeated measures ANOVA, and found a nonsignificant interaction (p = 0.16). Nonetheless, the analyses were consistent in direction with the results of the ANOVAs performed on the learning measures. We suspect that the additional variance introduced into these more complex ANOVA models resulted in less observed power.