Neural bases of risky decisions involving nicotine vapor versus monetary reward
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ABSTRACT:
SUBMITTER: Modak P
PROVIDER: S-EPMC8591353 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The dysfunctions of the mesolimbic cortical reward circuit have been proposed to contribute to migraine pain. Although supporting empirical evidence was mainly found in connection with primary rewards or in chronic migraine where the pain experience is (almost) constant. Our goal however was to investigate the neural correlates of secondary reward/loss anticipation and consumption using the monetary incentive delay task in 29 episodic migraine patients and 41 headache-free controls. Migraine patients showed decreased activation in one cluster covering the right inferior frontal gyrus during reward consumption compared to controls. We also found significant negative correlation between the time of the last migraine attack before the scan and activation of the parahippocampal gyrus and the right hippocampus yielded to loss anticipation. During reward/loss consumption, a relative increase in the activity of the visual areas was observed the more time passed between the last attack and the scan session. Our results suggest intact reward/loss anticipation but altered reward consumption in migraine, indicating a decreased reactivity to monetary rewards. The findings also raise the possibility that neural responses to loss anticipation and reward/loss consumption could be altered by the proximity of the last migraine attack not just during pre-ictal periods, but interictally as well.
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Project description:Being characterized by reduced pleasure from social interaction, social anhedonia constitutes a transdiagnostic marker for various psychiatric disorders. However, the neural portrait of social anhedonia remains elusive because of heterogeneities of reward type and reward dynamics in previous studies. The present event-related potential study investigated neural dynamics in response to monetary and social rewards in social anhedonia. Event-related potential responses were examined when a high social anhedonia (HSA, N = 23) group and a low social anhedonia (LSA, N = 26) group were anticipating and consuming social and monetary rewards. LSA but not HSA participants showed an increased stimulus-preceding negativity (anticipatory phase) and and increased reward positivity (consummatory phase) for monetary as compared with social rewards. This group difference could spring from an increased relevance of social rewards or a general decline in affective responding due to a potential association between social anhedonia and depression. Our findings provide preliminary evidence for neural aberrations of the reward system in social anhedonia, which is contingent upon reward type and reward dynamics.
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Project description:IntroductionPain catastrophizing, a measure of an individual's negative emotional and cognitive appraisals of pain, has been included as a key treatment target in many psychological interventions for pain. However, the neural correlates of pain catastrophizing have been understudied. Prior neuroimaging evidence suggests that adults with pain show altered reward processing throughout the mesocorticolimbic reward circuitry.MethodsIn this study, we tested the association between Pain Catastrophizing Scale (PCS) scores and neural activation to the Monetary Incentive Delay (MID) reward neuroimaging task in 94 adults reporting a range of pain, insomnia, and mood symptoms.ResultsResults indicated that PCS score but not pain intensity was significantly associated with blunted activation in the caudate and putamen in response to feedback of successful vs. unsuccessful trials on the MID task. Mediation analyses indicated that PCS score fully mediated the relationship between depression symptoms and reward activation.DiscussionThese findings provide evidence that pain catastrophizing is independently associated with altered striatal function apart from depression symptoms and pain intensity. Thus, in individuals experiencing pain and/or co- morbid conditions, reward dysfunction is directly related to pain catastrophizing.
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Project description:Contrary to the widespread belief that people are positively motivated by reward incentives, some studies have shown that performance-based extrinsic reward can actually undermine a person's intrinsic motivation to engage in a task. This "undermining effect" has timely practical implications, given the burgeoning of performance-based incentive systems in contemporary society. It also presents a theoretical challenge for economic and reinforcement learning theories, which tend to assume that monetary incentives monotonically increase motivation. Despite the practical and theoretical importance of this provocative phenomenon, however, little is known about its neural basis. Herein we induced the behavioral undermining effect using a newly developed task, and we tracked its neural correlates using functional MRI. Our results show that performance-based monetary reward indeed undermines intrinsic motivation, as assessed by the number of voluntary engagements in the task. We found that activity in the anterior striatum and the prefrontal areas decreased along with this behavioral undermining effect. These findings suggest that the corticobasal ganglia valuation system underlies the undermining effect through the integration of extrinsic reward value and intrinsic task value.
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Project description:BackgroundAccidental injury and homicide, relatively common among adolescents, often follow risky behaviors; those are done more by boys and by adolescents with greater behavioral disinhibition (BD).HypothesisNeural processing during adolescents' risky decision-making will differ in youths with greater BD severity, and in males vs. females, both before cautious behaviors and before risky behaviors.Methodology/principal findings81 adolescents (PATIENTS with substance and conduct problems, and comparison youths (Comparisons)), assessed in a 2 x 2 design (PatientsComparisons x Male:Female) repeatedly decided between doing a cautious behavior that earned 1 cent, or a risky one that either won 5 or lost 10 cents. Odds of winning after risky responses gradually decreased. Functional magnetic resonance imaging captured brain activity during 4-sec deliberation periods preceding responses. Most neural activation appeared in known decision-making structures. PATIENTS, who had more severe BD scores and clinical problems than Comparisons, also had extensive neural hypoactivity. Comparisons' greater activation before cautious responses included frontal pole, medial prefrontal cortex, striatum, and other regions; and before risky responses, insula, temporal, and parietal regions. Males made more risky and fewer cautious responses than females, but before cautious responses males activated numerous regions more than females. Before risky behaviors female-greater activation was more posterior, and male-greater more anterior.Conclusions/significanceNeural processing differences during risky-cautious decision-making may underlie group differences in adolescents' substance-related and antisocial risk-taking. Patients reported harmful real-life decisions and showed extensive neural hypoactivity during risky-or-cautious decision-making. Males made more risky responses than females; apparently biased toward risky decisions, males (compared with females) utilized many more neural resources to make and maintain cautious decisions, indicating an important risk-related brain sexual dimorphism. The results suggest new possibilities for prevention and management of excessive, dangerous adolescent risk-taking.
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Project description:Reward seeking is ubiquitous and adaptive in humans. But excessive reward seeking behavior, such as chasing monetary rewards, may lead to diminished subjective well-being. This study examined whether individuals trained in mindfulness meditation show neural evidence of lower susceptibility to monetary rewards. Seventy-eight participants (34 meditators, 44 matched controls) completed the monetary incentive delay task while undergoing functional magnetic resonance imaging. The groups performed equally on the task, but meditators showed lower neural activations in the caudate nucleus during reward anticipation, and elevated bilateral posterior insula activation during reward anticipation. Meditators also evidenced reduced activations in the ventromedial prefrontal cortex during reward receipt compared with controls. Connectivity parameters between the right caudate and bilateral anterior insula were attenuated in meditators during incentive anticipation. In summary, brain regions involved in reward processing-both during reward anticipation and receipt of reward-responded differently in mindfulness meditators than in nonmeditators, indicating that the former are less susceptible to monetary incentives.
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Project description:Internet Gaming Disorder (IGD) has been considered a potential behavioral or non-substance addiction that requires further investigation. Recognition of the commonalities between IGD and Substance Use disorders (SUD) would be of great help to better understand the basic mechanisms of addictive behaviors and excessive Internet gaming. However, little research has targeted a straightforward contrast between IGD and SUD on neuropsychological aspects. The present study thus aimed to explore the associations of reward processing and inhibitory control with IGD and nicotine dependence (ND) in young adults. Fifty-eight IGD and 53 ND individuals, as well as 57 age- and gender-matched healthy controls, were assessed with a series of measurements including the Delay-discounting Test (DDT), Probability Discounting Test (PDT), the Stroop Color-Word Task, a revised Go/No Go Task, and the Barratt Impulsiveness Scale (BIS-11). Multivariate analysis of variance (mANOVA) models revealed that both IGD and ND groups scored higher than healthy controls on the BIS-11 attentional, motor, and non-planning impulsiveness (Cohen's d = 0.41-1.75). Higher degrees of delay discounting on the DDT were also found in IGD and ND groups compared to healthy controls (Cohen's d = 0.53-0.69). Although IGD group did not differ from healthy controls on the PDT, ND group had a lower degree of probability discounting than healthy controls (Cohen's d = 0.55), suggesting a reduction in risk aversion. Furthermore, ND subjects showed a lower correct accuracy in the incongruent trials of the Stroop task than healthy controls (Cohen's d = 0.61). On the Go/No Go task, both IGD and ND groups had a lower correct accuracy in the No-Go trials than healthy controls (Cohen's d = 1.35-1.50), indicating compromised response inhibition. These findings suggested that IGD was linked to both anomalous reward discounting and dysfunctional inhibitory control, which was comparable with one typical SUD category (i.e., ND). This study might promote a better understanding of the pathogenesis of IGD as a potential addictive disorder similar to SUD.
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Project description:BackgroundRobust evidence links sleep and circadian rhythm disturbances to alcohol use and alcohol-related problems, with a growing literature implicating reward-related mechanisms. However, the extant literature has been limited by cross-sectional designs, self-report or behavioral proxies for circadian timing, and samples without substantive alcohol use. Here, we employed objective measures of sleep and circadian rhythms, and an intensive prospective design, to assess whether circadian alignment predicts the neural response to reward in a sample of late adolescents reporting regular alcohol use.MethodsParticipants included 31 late adolescents (18-22 y/o; 19 female participants) reporting weekly alcohol use. Participants completed a 14-day protocol including pre- and post-weekend (Thursday and Sunday) circadian phase assessments via the dim light melatonin onset (DLMO), in counterbalanced order. Sleep-wake timing was assessed via actigraphy. Circadian alignment was operationalized as the DLMO-midsleep interval; secondary analyses considered social jet lag based on weekday-weekend differences in midsleep or DLMO. Neural response to reward (anticipation and outcome) was assessed via a monetary reward fMRI task (Friday and Monday scans). Alcohol use was assessed at baseline and via ecological momentary assessment. Mean BOLD signal was extracted from two regions-of-interest (striatum and medial prefrontal cortex, mPFC) for analyses in regression models, accounting for age, sex, racial identity, and scan order.ResultsIn primary analyses, shorter DLMO-midsleep intervals (i.e., greater misalignment) on Thursday predicted lower striatal and mPFC responses to anticipated reward, but not reward outcome, on Friday. Lower neural (striatum and mPFC) responses to anticipated reward on Friday correlated with more binge-drinking episodes at baseline, but were not associated with alcohol use in the post-scan weekend. In secondary analyses, greater social jet lag (particularly larger weekend delays in midsleep or DLMO) was associated with lower neural responses to reward anticipation on Monday.ConclusionFindings provide preliminary evidence of proximal associations between objectively determined circadian alignment and the neural response to anticipated monetary reward, which is linked in turn to patterns of problematic drinking. Replication in a larger sample and experimental designs will be important next steps to determining the extent to which circadian misalignment influences risk for alcohol involvement via alterations in reward function.
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Project description:The ubiquitous and intense nature of stress responses necessitate that we understand how they affect decision-making. Despite a number of studies examining risky decision-making under stress, it is as yet unclear whether and in what way stress alters the underlying processes that shape our choices. This is in part because previous studies have not separated and quantified dissociable valuation and decision-making processes that can affect choices of risky options, including risk attitudes, loss aversion, and choice consistency, among others. Here, in a large, fully-crossed two-day within-subjects design, we examined how acute stress alters risky decision-making. On each day, 120 participants completed either the cold pressor test or a control manipulation with equal probability, followed by a risky decision-making task. Stress responses were assessed with salivary cortisol. We fit an econometric model to choices that dissociated risk attitudes, loss aversion, and choice consistency using hierarchical Bayesian techniques to both pool data and allow heterogeneity in decision-making. Acute stress was found to have no effect on risk attitudes, loss aversion, or choice consistency, though participants did become more loss averse and more consistent on the second day relative to the first. In the context of an inconsistent previous literature on risk and acute stress, our findings provide strong and specific evidence that acute stress does not affect risk attitudes, loss aversion, or consistency in risky monetary decision-making.
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Project description:One well-known phenotypic risk factor for the development of alcohol use disorder is sensitivity to the rewarding effects of alcohol. In the present study, we examined whether individuals who are sensitive to alcohol reward are also sensitive to nondrug rewards, thereby reflecting a broader individual difference risk factor. Specifically, we tested the hypothesis that subjective response to acute rewarding effects of alcohol would be related to neural activation during monetary reward receipt relative to loss (in the absence of alcohol). Community-recruited healthy young social drinkers (N = 58) completed four laboratory sessions in which they received alcohol (0.8 g/kg) and placebo in alternating order under double-blind conditions, providing self-report measures of subjective response to alcohol at regular intervals. At a separate visit 1-3 weeks later, they completed a reward-guessing game, the 'Doors' task, during fMRI in a drug-free state. Participants who reported greater motivation (i.e., wanting) to consume more alcohol after a single moderate dose of alcohol also exhibited greater neural activation in the bilateral ventral caudate and the nucleus accumbens during reward receipt relative to loss. Striatal activation was not related to other subjective ratings including alcohol-induced sedation, stimulation, or pleasure (i.e., feeling, liking). Our study is the first to show that measures of alcohol reward are related to neural indices of monetary reward in humans. These results support growing evidence that individual differences in responses to drug and nondrug reward are linked and together form a risk profile for drug use or abuse, particularly in young adults.
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