Effects of social and nonsocial reward on executive function in preschoolers.
ABSTRACT: INTRODUCTION:Executive function, a set of higher order cognitive skills underlying goal-directed behaviors, develops rapidly during preschool years. Reward increases executive function engagement in adolescents and adults. However, there is still a scarcity of data on how reward affects executive function in young children. The present study examines whether different incentive types contribute differently to executive function performance and neural activity in children. METHODS:Twenty-five preschoolers of 5-6 years old were provided an incentive Go/No-go task, comparing social, nonsocial, and nonreward conditions. Activations in the prefrontal regions during the tasks were measured using functional near-infrared spectroscopy. RESULTS:The results revealed that social reward enhanced right prefrontal activations in young children. In contrast to adult literature, younger children did not show any significant differences in executive function performance across conditions. CONCLUSION:This study expands our understanding of motivation and EF engagement in preschoolers. Specifically, social reward enhanced prefrontal activations in young children. The implications and recommendations for future research are discussed.
Project description:Low executive function (EF) during early childhood is a major risk factor for developmental delay, academic failure, and social withdrawal. Susceptible genes may affect the molecular and biological mechanisms underpinning EF. More specifically, genes associated with the regulation of prefrontal dopamine may modulate the response of prefrontal neurons during executive control. Several studies with adults and older children have shown that variants of the catechol-O-methyltransferase (COMT) gene are associated with behavioral performance and prefrontal activations in EF tasks. However, the effect of the COMT genotype on prefrontal activations during EF tasks on young children is still unknown. The present study examined whether a common functional polymorphism (Val158Met) in the COMT gene was associated with prefrontal activations and cognitive shifting in 3- to 6-year-old children. The study revealed that, compared with children with at least one Met allele (Met/Met and Met/Val), children who were Val homozygous (i) were more able to flexibly switch rules in cognitive shifting tasks and (ii) exhibited increased activations in lateral prefrontal regions during these tasks. This is the first evidence that demonstrates the relationship between a gene polymorphism and prefrontal activations in young children. It also indicates that COMT Val homozygosity may be advantageous for cognitive shifting and prefrontal functions, at least during early childhood, and children who possess this variant may have a lower risk of developing future cognitive and social development issues.
Project description:Socioeconomic status (SES) has a powerful influence on cognitive, social and brain development. Children from low-SES backgrounds show poor executive function (EF). However, it is unclear if there is a SES-dependent disparity in functional brain development. The present study examined whether the SES of preschool children (N?=?93) is associated with prefrontal activation during cognitive shifting tasks as measured by near-infrared spectroscopy. Low-SES children did not show activation in lateral prefrontal regions during the tasks, whereas middle- and high-SES children showed prefrontal activations, although no differences were found in terms of behavioural performance. These results suggest that SES can affect the functional development of the prefrontal regions. In this study, we discuss the practical implications of the results.
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.
Project description:Background:Reward seeking and avoidance of punishment are key motivational processes. Brain-imaging studies often use the Monetary Incentive Delay Task (MIDT) to evaluate motivational processes involved in maladaptive behavior. Although the bulk of research has been done on the MIDT reward events, little is known about the neural basis of avoidance of punishment. Therefore, we conducted a meta-analysis of brain activations during anticipation and receipt of monetary losses in healthy controls. Methods:All functional neuro-imaging studies using the MIDT in healthy controls were retrieved using PubMed, Google Scholar & EMBASE databases. Functional neuro-imaging data was analyzed using the Seed-based d Mapping Software. Results:Thirty-five studies met the inclusion criteria, comprising 699 healthy adults. In both anticipation and loss outcome phases, participants showed large and robust activations in the bilateral striatum, (anterior) insula, and anterior cingulate gyrus relatively to Loss > Neutral contrast. Although relatively similar activation patterns were observed during the two event types, they differed in the pattern of prefrontal activations: ventro-lateral prefrontal activations were observed during loss anticipation, while medial prefrontal activations were observed during loss receipt. Discussion:Considering that previous meta-analyses highlighted activations in the medial prefrontal cortex/anterior cingulate cortex, the anterior insula and the ventral striatum, the current meta-analysis highlighted the potential specificity of the ventro-lateral prefrontal regions, the median cingulate cortex and the amygdala in the loss events. Future studies can rely on these latter results to examine the neural correlates of loss processing in psychiatric populations characterized by harm avoidance or insensitivity to punishment.
Project description:Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction.
Project description:RATIONALE:Oxytocin is a neuropeptide widely recognized for its role in regulating social and reproductive behavior. Increasing evidence from animal models suggests that oxytocin also modulates reward circuitry in non-social contexts, but evidence in humans is lacking. OBJECTIVES:We examined the effects of oxytocin administration on reward circuit function in 18 healthy men as they performed a monetary incentive task. METHODS:The blood oxygenation level-dependent (BOLD) signal was measured using functional magnetic resonance imaging in the context of a randomized, double-blind, placebo-controlled, crossover trial of intranasal oxytocin. RESULTS:We found that oxytocin increases the BOLD signal in the midbrain (substantia nigra and ventral tegmental area) during the late phase of the hemodynamic response to incentive stimuli. Oxytocin's effects on midbrain responses correlated positively with its effects on positive emotional state. We did not detect an effect of oxytocin on responses in the nucleus accumbens. Whole-brain analyses revealed that oxytocin attenuated medial prefrontal cortical deactivation specifically during anticipation of loss. CONCLUSIONS:Our findings demonstrate that intranasal administration of oxytocin modulates human midbrain and medial prefrontal function during motivated behavior. These findings suggest that endogenous oxytocin is a neurochemical mediator of reward behaviors in humans-even in a non-social context-and that the oxytocinergic system is a potential target of pharmacotherapy for psychiatric disorders that involve dysfunction of reward circuitry.
Project description:BACKGROUND:Research in adolescents and adults has suggested that altered neural processing of reward following early life adversity is a highly promising depressive intermediate phenotype. However, very little is known about how stress response, neural processing of reward, and depression are related in very young children. The present study examined the concurrent associations between cortisol response following a stressor, functional brain activity to reward, and depression severity in children 4 to 6 years old. METHODS:Medication-naïve children 4 to 6 years old (N = 52) participated in a study using functional magnetic resonance imaging to assess neural reactivity to reward, including gain, loss, and neutral outcomes. Parent-reported child depression severity and child cortisol response following stress were also measured. RESULTS:Greater caudate and medial prefrontal cortex reactivity to gain outcomes and increased amygdala reactivity to salient (i.e., both gain and loss) outcomes were observed. Higher total cortisol output following a stressor was associated with increased depression severity and reduced amygdala reactivity to salient outcomes. Amygdala reactivity was also inversely associated with depression severity and was found to mediate the relationship between cortisol output and depression severity. CONCLUSIONS:Results suggest that altered neural processing of reward is already related to increased cortisol output and depression severity in preschoolers. These results also demonstrate an important role for amygdala function as a mediator of this relationship at a very early age. Our results further underscore early childhood as an important developmental period for understanding the neurobiological correlates of early stress and increased risk for depression.
Project description:It is increasingly appreciated that executive control processes need to be understood in terms of motivational as well as cognitive mechanisms. The current study examined the impact of performance-contingent reward incentives (monetary bonuses) on neural activity dynamics during cued task-switching performance. Behavioral measures indicated that performance was improved and task-switch costs selectively reduced on incentive trials. Trial-by-trial fluctuations in incentive value were associated with activation in reward-related brain regions (dopaminergic midbrain, paracingulate cortex) and also modulated the dynamics of switch-selective activation in the brain cognitive control network. Within lateral prefrontal cortex (PFC), both additive (inferior frontal junction) and interactive [dorsolateral PFC (DLPFC)] incentive effects were observed. In DLPFC, incentive modulation of activation predicted task-switching behavioral performance, but with hemispherically dissociable effects. Furthermore, in left DLPFC, incentive modulation specifically enhanced task-cue-related activation, and this activation in turn predicted that the trial would be subsequently rewarded (because of optimal performance). The results suggest that motivational incentives have a selective effect on brain regions that subserve cognitive control processes during task-switching and, moreover, that one mechanism of effect might be the enhancement of cue-related task preparation within left DLPFC.
Project description:Mesocorticolimbic neurocircuitry and impulsivity have both been implicated in pathological gambling (PG) and in reward processing. However, the neural underpinnings of specific phases of reward and loss processing in PG and their relationships to impulsivity remain only partially understood. The present functional magnetic resonance imaging study examined brain activity associated with different phases of reward and loss processing in PG. Given an inverse relationship between ventral striatal recruitment during anticipation of monetary rewards and impulsivity in alcohol dependence, the current study explored whether a similar association might also be present in PG.Fourteen adults with PG and 14 control comparison participants performed the Monetary Incentive Delay Task to identify brain activation changes associated with reward/loss prospect, reward/loss anticipation, and reward/loss notification. Impulsivity was assessed separately using the Barratt Impulsiveness Scale.Relative to the control comparison group, the PG group exhibited significantly reduced activity in the ventromedial prefrontal cortex, insula, and ventral striatum during several phases, including the prospect and anticipation phases of both gains and losses. Activity in the ventral striatum correlated inversely with levels of impulsivity in PG participants, consistent with prior findings in alcohol dependence.Relatively decreased activity in corticostriatal neurocircuitry during multiple phases of reward processing suggests consistent alterations in neurocircuitry underlying incentive valuation and loss prediction. Together with findings in alcohol dependence, these results suggest that impulsive tendencies in addictions may be reflected in diminished ventral striatal activations to reward anticipation and may represent targets for treatment development in addictions.
Project description:Although altered function in neural reward circuitry is widely proposed in models of addiction, more recent conceptual views have emphasized the role of disrupted response in prefrontal regions. Changes in regions such as the orbitofrontal cortex, medial prefrontal cortex, and dorsolateral prefrontal cortex are postulated to contribute to the compulsivity, impulsivity, and altered executive function that are central to addiction. In addition, few studies have examined function in these regions during young adulthood, when exposure is less chronic than in typical samples of alcohol-dependent adults. To address these issues, we examined neural response and functional connectivity during monetary reward in 24 adults with alcohol dependence and 24 psychiatrically healthy adults. Adults with alcohol dependence exhibited less response to the receipt of monetary reward in a set of prefrontal regions including the medial prefrontal cortex, lateral orbitofrontal cortex, and dorsolateral prefrontal cortex. Adults with alcohol dependence also exhibited greater negative correlation between function in each of these regions and that in the nucleus accumbens. Within the alcohol-dependent group, those with family history of alcohol dependence exhibited lower mPFC response, and those with more frequent drinking exhibited greater negative functional connectivity between the mPFC and the nucleus accumbens. These findings indicate that alcohol dependence is associated with less engagement of prefrontal cortical regions, suggesting weak or disrupted regulation of ventral striatal response. This pattern of prefrontal response and frontostriatal connectivity has consequences for the behavior patterns typical of addiction. Furthermore, brain-behavior findings indicate that the potential mechanisms of disruption in frontostriatal circuitry in alcohol dependence include family liability to alcohol use problems and more frequent use of alcohol. In all, these findings build on the extant literature on reward-circuit function in addiction and suggest mechanisms for disrupted function in alcohol dependence.