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Reward Processing (reward + processing)
Selected AbstractsGlutamate-Dopamine Cotransmission and Reward Processing in AddictionALCOHOLISM, Issue 9 2006Christopher C. Lapish While Dale's principle of "one neuron, one neurotransmitter" has undergone revisions to incorporate evidence of the corelease of atypical neurotransmitters such as neuropeptides, the corelease of classical neurotransmitters has only recently been realized. Surprisingly, numerous studies now indicate that the corelease of neurotransmitters in the mammalian central nervous system is not an obscure and rare phenomenon but is widespread and involves most classical neurotransmitters systems. However, the suggestion that glutamate can be coreleased with dopamine (DA) has remained controversial. Furthermore, glutamate-DA cotransmission has not yet been seriously considered in the context of the neurocircuitry of addiction. If glutamate is in fact coreleased with DA as some evidence now suggests, this may have significant implications for advancing our understanding of the interactive role that these 2 neurotransmitters play in cognitive and reward processes. In this commentary, we review the evidence for and against glutamate as a cotransmitter and discuss the potential role of glutamate-DA corelease in addiction. In particular, we describe a recently proposed model in which coreleased glutamate transmits a temporally precise prediction error signal of reward described by Schultz et al., whereas the function of coreleased DA is to exert prolonged modulatory influences on neuronal activity. In addition, we suggest that as alcohol consumption transitions from recreational use to addiction, there is a corresponding transition in the reward valence signal from better than predicted to worse than predicted. [source] B.O.L.D. Statements on Human Reward ProcessingPSYCHOPHYSIOLOGY, Issue 2010Article first published online: 5 AUG 2010 First page of article [source] Incentive-elicited mesolimbic activation and externalizing symptomatology in adolescentsTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 7 2010James M. Bjork Background:, Opponent-process theories of externalizing disorders (ExD) attribute them to some combination of overactive reward processing systems and/or underactive behavior inhibition systems. Reward processing has been indexed by recruitment of incentive-motivational neurocircuitry of the ventral striatum (VS), including nucleus accumbens (NAcc). Methods:, We used functional magnetic resonance imaging (fMRI) with an incentive task to determine whether externalizing symptomatology in adolescence is correlated with an enhanced VS recruitment by cues for rewards, or by deliveries of rewards. Twelve community-recruited adolescents with externalizing disorders (AED) and 12 age/gender-matched controls responded to targets to win or avoid losing $0, $0.20, $1, $5, or an unknown amount (ranging from $0.20 to $5). Results:, Cues to respond for rewards activated the NAcc (relative to cues for no incentive), in both subject groups similarly, with greatest NAcc recruitment by cues for the largest reward. Loss-anticipatory NAcc signal increase was detected in a volume-of-interest analysis , but this increase occurred only in trials when subjects hit the target. Relative to controls, AED showed significantly elevated NAcc activation by a linear contrast between reward notification versus notification of failure to win reward. In a post hoc reanalysis, VS and pregenual anterior cingulate activation by the reward versus non-reward outcome contrast also directly correlated with Child Behavior Checklist (CBCL) Externalizing total scores (across all subjects) in lieu of a binary diagnosis. Finally, both groups showed right insula activation by loss notifications (contrasted with avoided losses). Conclusions:, Externalizing behavior, whether assessed dimensionally with a questionnaire, or in the form of a diagnostic categorization, is associated with an exaggerated limbic response to outcomes of reward-directed behavior. This could be a neurobiological signature of the behavioral sensitivity to laboratory reward delivery that is characteristic of children with externalizing symptomatology. Of interest is future research on incentive-motivational processing in more severe, clinically referred AED. [source] The utility of behavioral models and modules in molecular analyses of social behaviorGENES, BRAIN AND BEHAVIOR, Issue 3 2008Andrew B. Barron It is extremely difficult to trace the causal pathway relating gene products or molecular pathways to the expression of behavior. This is especially true for social behavior, which being dependent on interactions and communication between individuals is even further removed from molecular-level events. In this review, we discuss how behavioral models can aid molecular analyses of social behavior. Various models of behavior exist, each of which suggest strategies to dissect complex behavior into simpler behavioral ,modules.' The resulting modules are easier to relate to neural processes and thus suggest hypotheses for neural and molecular function. Here we discuss how three different models of behavior have facilitated understanding the molecular bases of aspects of social behavior. We discuss the response threshold model and two different approaches to modeling motivation, the state space model and models of reinforcement and reward processing. The examples we have chosen illustrate how models can generate testable hypotheses for neural and molecular function and also how molecular analyses probe the validity of a model of behavior. We do not champion one model over another; rather, our examples illustrate how modeling and molecular analyses can be synergistic in exploring the molecular bases of social behavior. [source] Increased Activation of the ACC During a Spatial Working Memory Task in Alcohol-Dependence Versus Heavy Social DrinkingALCOHOLISM, Issue 5 2010Sabine Vollstädt-Klein Background:, Activation of the anterior cingulate cortex (ACC) in a spatial working memory task has been associated with risk factors for alcohol use disorders such as low alcohol effects and positive alcohol expectations in adolescents. To transfer these results into adults, we used the same task in adults. Methods:, During functional magnetic resonance imaging, 12 light social, 7 heavy social, and 11 non-abstinent-dependent alcohol drinkers performed a spatial working memory task and completed measures of automatic alcohol-related thoughts and behavior (Obsessive,Compulsive Drinking Scale,OCDS), alcohol use of the last 90 days, and general intelligence. Results:, Behavioral performance in the spatial working memory task was not significantly different in all 3 groups. Controlling for differences in general intelligence alcohol-dependent participants showed a higher task-related activation of the dorsal ACC (dACC) in comparison with light and heavy social drinkers. Measures of the OCDS were positively correlated with the activation in the left hippocampus and right thalamus in all participants. Conclusions:, Our results support the findings of increased dACC activation during a spatial working memory task as a risk factor for alcohol dependence. Increased task-related activation in the dACC was only observed in alcohol-dependent participants and not in heavy social drinkers with comparable alcohol consumption. Furthermore, the absence of behavioral performance differences between groups as well as an association between dACC activation and working memory performance indicates subtle working memory deficits. Low capacity of working memory has been linked to more automatic and less self-regulated behavior in studies on natural reward processing. Therefore, additional neural activation during performance of the non-alcohol-related working memory task in participants with higher OCDS values in the left hippocampus and the right thalamus may be a consequence of decreased neural capacity because of distracting alcohol-related thoughts. [source] Individual Differences in Alcohol Drinking Frequency Are Associated With Electrophysiological Responses to Unexpected NonrewardsALCOHOLISM, Issue 4 2010Ingmar H. A. Franken Background:, It has been suggested that alcohol use is related to sensitivity of the reward system. Although there are several studies using self-reported measures supportive of this notion, objective biological data in humans on this issue are lacking. Aims:, This study is designed to test whether alcohol drinking frequency is associated with electrophysiological indices of reward processing. Materials and Methods:, In a passive gambling task, stimuli predicted the presence (reward) and absence (nonreward) of rewards resulting in P2 and medial frontal negativity (MFN) indices of reward processing. Forty-seven undergraduate students were asked about their habitual drinking frequency and the P2 and MFN to stimuli predicting reward were measured. Results:, Most importantly, the MFN to unpredicted nonrewards at the frontal midline (Fz) location correlated significantly with drinking frequency, with frequent drinkers showing larger MFN amplitudes. The results did not show a significant association between frequency and alcohol drinking and P2. Discussion:, Although several studies showing increased reward-sensitivity in addictive behaviors, the present results indicate that, in frequent alcohol drinkers, electrophysiological responsiveness is particularly activated by unpredicted nonrewards. In general, this may point to the involvement of the reward system in alcohol drinking frequency. Conclusion:, More specifically, the results demonstrate an increased vulnerability of high frequency drinkers to signals of (frustrative) nonrewards. [source] Abnormal activity in reward brain circuits in human narcolepsy with cataplexyANNALS OF NEUROLOGY, Issue 2 2010Aurélie Ponz PhD Objective Hypothalamic hypocretins (or orexins) regulate energy metabolism and arousal maintenance. Recent animal research suggests that hypocretins may also influence reward-related behaviors. In humans, the loss of hypocretin-containing neurons results in a major sleep-wake disorder called narcolepsy-cataplexy, which is associated with emotional disturbances. Here, we aim to test whether narcoleptic patients show an abnormal pattern of brain activity during reward processing. Methods We used functional magnetic resonance imaging in 12 unmedicated patients with narcolepsy-cataplexy to measure the neural responses to expectancy and experience of monetary gains and losses. We statistically compared the patients' data with those obtained in a group of 12 healthy matched controls. Results and Interpretation Our results reveal that activity in the dopaminergic ventral midbrain (ventral tegmental area) was not modulated in narcolepsy-cataplexy patients during high reward expectancy (unlike controls), and that ventral striatum activity was reduced during winning. By contrast, the patients showed abnormal activity increases in the amygdala and in dorsal striatum for positive outcomes. In addition, we found that activity in the nucleus accumbens and the ventral-medial prefrontal cortex correlated with disease duration, suggesting that an alternate neural circuit could be privileged over the years to control affective responses to emotional challenges and compensate for the lack of influence from ventral midbrain regions. Our study offers a detailed picture of the distributed brain network involved during distinct stages of reward processing and shows for the first time, to our knowledge, how this network is affected in hypocretin-deficient narcoleptic patients. ANN NEUROL 2010;67:190,200 [source] | |||||||||||||