Search

Adolescence is critical period of neurocognitive development as well as increased prevalence of mood pathology. This cross-sectional study replicated developmental patterns of neurocognition and tested whether mood symptoms moderated developmental effects. Participants were 419 adolescents (n=246 with current mood disorders) who completed reward learning and executive functioning tasks, and reported on age, puberty, and mood symptoms. Structural equation modeling revealed a quadratic relationship between puberty and reward learning performance that was moderated by symptom severity: in early puberty, adolescents reporting higher manic symptoms exhibited heightened reward learning performance (better maximizing of rewards on learning tasks), whereas adolescents reporting elevated anhedonia showed blunted reward learning performance. Models also showed a linear relationship between age and executive functioning that was moderated by manic symptoms: adolescents reporting higher mania showed poorer executive functioning at older ages. Findings suggest neurocognitive development is altered in adolescents with mood pathology and suggest directions for longitudinal studies.

Several studies of reward processing in schizophrenia have shown reduced sensitivity to positive, but not negative, outcomes although inconsistencies have been reported. In addition, few studies have investigated whether patients show a relative deficit to social versus nonsocial rewards, whether deficits occur across the spectrum of psychosis, or whether deficits relate to negative symptoms and functioning. This study examined probabilistic implicit learning via two visually distinctive slot machines for social and nonsocial rewards in 101 outpatients with diverse psychotic disorders and 48 community controls. The task consisted of two trial types: positive (optimal to choose a positive vs. neutral machine) and negative (optimal to choose a neutral vs. negative machine), with two reward conditions: social (faces) and nonsocial (money) reward conditions. A significant group X trial type interaction indicated that controls performed better on positive than negative trials, whereas patients showed the opposite pattern of better performance on negative than positive trials. In addition, both groups performed better for social than nonsocial stimuli, despite lower overall task performance in patients. Within patients, worse performance on negative trials showed significant, small-to-moderate correlations with motivation and pleasure-related negative symptoms and social functioning. The current findings suggest reward processing disturbances, particularly decreased sensitivity to positive outcomes, extend beyond schizophrenia to a broader spectrum of psychotic disorders and relate to important clinical outcomes.

BackgroundAtypical inflammatory biology is gaining evidence as a risk factor for mood psychopathology; however, little work has attempted to integrate inflammation into extant psychosocial frameworks of risk. Recent work using secondary data analysis has investigated the possibility of an immunocognitive model of mood disorders, in which cognitive vulnerabilities (i.e., rumination on positive or negative affect) increase the effect that arousal-related characteristics (e.g., reward sensitivity) have on inflammatory biology in ways that may confer risk for depression and hypo/mania symptoms. Project MIME (Motivation, Inflammation, and Mood in Emerging Adults) was designed to test this model in the context of a novel, reward-salient stressor (the Anger Incentive Delay Task, AIDT).MethodsThis NIMH-funded study will result in a dataset of approximately 100 college undergraduates from a large university in Pennsylvania, United States of America. Eligible participants are recruited from an online screener, have to be 18-22 years old, fluent in English, and successfully answer several items designed to test whether participants randomly answer questions on the screener. Eligible participants are invited to an in-person visit in which they completed the AIDT, blood draws pre- and 50 minutes post-AIDT, and self-report questionnaires. Participants also complete a set of online questionnaires two weeks after the in-person visit.DiscussionConsistent with calls from the NIH director, this study seeks to diversify the tools used in stress research by validating a novel reward-salient stressor (in contrast to the field's reliance on social stressors) with respect to affective and immunological stress reactivity. In addition to this methodological goal, Project MIME is the first study specifically designed to test the immunocognitive model of mood psychopathology. Given the integration of several malleable treatment targets (approach behavior, emotion regulation, inflammation) into this model, results from this study could inform comprehensive, flexible intervention strategies for mood disorder prevention and treatment.

Animal-based measures reflecting the welfare state of individuals are critical for ensuring the well-being of animals under human care. Anticipatory behavior is one potential animal-based measure that has gained traction in recent years, as it is theorized to relate to animals' reward sensitivity. It is of particular interest as an assessment for animals living under human care, as the predictability of the captive environment lends itself to the development of this class of behaviors. Animals are likely to exhibit anticipation in locations related to the anticipated event, often in temporally predictable time frames, and before specific contexts they experience in their day-to-day management. In this sense and under certain circumstances, anticipatory behaviors are likely to drive observed behavioral or space use patterns of animals under human care. Drawing conclusions from such data without identifying anticipation may result in misleading conclusions. Here we discuss how space, time, and context are related to patterns of anticipatory behaviors in animals under human care, how unidentified anticipation may alter conclusions regarding animal behavior or welfare under certain circumstances.

BackgroundAnhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing.MethodsHealthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor.ResultsStress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6.ConclusionsContrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting.Clinical trial registrationNCT03828604.

BackgroundAnhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing.MethodsHealthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor.ResultsStress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6.ConclusionsContrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting.Clinical trial registrationNCT03828604.

BackgroundAnhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing.MethodsHealthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor.ResultsStress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6.ConclusionsContrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting.Clinical trial registrationNCT03828604.

RationaleDrug addiction can be described as aberrant allocation of effort toward acquiring drug, despite associated costs. It is unclear if this behavioral pattern results from an overvaluation of reward or to an altered sensitivity to costs.ObjectivePresent experiments assessed reward sensitivity and effortful choice in rats following 1 week of withdrawal from methamphetamine (mAMPH).MethodsRats were treated with either saline or an escalating dose mAMPH regimen, then tested after a week without the drug. In experiment 1, rats were given a free choice between water and various concentrations of sucrose solution to assess general reward sensitivity. In experiment 2, rats were presented with a choice between lever-pressing for sucrose pellets on a progressive ratio schedule or consuming freely-available chow.ResultsIn experiment 1, we found no differences in sucrose preference between mAMPH- and saline-pretreated rats. In experiment 2, when selecting between two options, mAMPH-pretreated rats engaged in less lever-pressing for sucrose pellets (p

A new virtual reality task was employed which uses preference for interpersonal distance to social stimuli to examine social motivation and emotion perception in children with Autism Spectrum Disorders. Nineteen high function children with higher functioning Autism Spectrum Disorder (HFASD) and 23 age, gender, and IQ matched children with typical development (TD) used a joy stick to position themselves closer or further from virtual avatars while attempting to identify six emotions expressed by the avatars, happiness, fear, anger, disgust, sadness, and surprise that were expressed at different levels of intensity. The results indicated that children with HFASD displayed significantly less approach behavior to the positive happy expression than did children with TD, who displayed increases in approach behavior to higher intensities of happy expressions. Alternatively, all groups tended to withdraw from negative emotions to the same extent and there were no diagnostic group differences in accuracy of recognition of any of the six emotions. This pattern of results is consistent with theory that suggests that some children with HFASD display atypical social-approach motivation, or sensitivity to the positive reward value of positive social-emotional events. Conversely, there was little evidence that a tendency to withdraw from social-emotional stimuli, or a failure to process social emotional stimuli, was a component of social behavior task performance in this sample of children with HFASD.