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Reward Processes (reward + process)
Selected AbstractsREVIEW: Reward sensitivity: issues of measurement, and achieving consilience between human and animal phenotypesADDICTION BIOLOGY, Issue 2 2010David N. Stephens ABSTRACT Reward is a concept fundamental to discussions of drug abuse and addiction. The idea that altered sensitivity to either drug,reward, or to rewards in general, contributes to, or results from, drug-taking is a common theme in several theories of addiction. However, the concept of reward is problematic in that it is used to refer to apparently different behavioural phenomena, and even to diverse neurobiological processes (reward pathways). Whether these different phenomena are different behavioural expressions of a common underlying process is not established, and much research suggests that there may be only loose relationships among different aspects of reward. Measures of rewarding effects of drugs in humans often depend upon subjective reports. In animal studies, such insights are not available, and behavioural measures must be relied upon to infer rewarding effects of drugs or other events. In such animal studies, but also in many human methods established to objectify measures of reward, many other factors contribute to the behaviour being studied. For that reason, studying the biological (including genetic) bases of performance of tasks that ostensibly measure reward cannot provide unequivocal answers. The current overview outlines the strengths and weaknesses of current approaches that hinder the conciliation of cross-species studies of the genetics of reward sensitivity and the dysregulation of reward processes by drugs of abuse. Some suggestions are made as to how human and animal studies may be made to address more closely homologous behaviours, even if those processes are only partly able to isolate ,reward' from other factors contributing to behavioural output. [source] Subjective neuronal coding of reward: temporal value discounting and riskEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2010Wolfram Schultz Abstract A key question in the neurobiology of reward relates to the nature of coding. Rewards are objects that are advantageous or necessary for the survival of individuals in a variety of environmental situations. Thus reward appears to depend on the individual and its environment. The question arises whether neuronal systems in humans and monkeys code reward in subjective terms, objective terms or both. The present review addresses this issue by dealing with two important reward processes, namely the individual discounting of reward value across temporal delays, and the processing of information about risky rewards that depends on individual risk attitudes. The subjective value of rewards decreases with the temporal distance to the reward. In experiments using neurophysiology and brain imaging, dopamine neurons and striatal systems discount reward value across temporal delays of a few seconds, despite unchanged objective reward value, suggesting subjective value coding. The subjective values of risky outcomes depend on the risk attitude of individual decision makers; these values decrease for risk-avoiders and increase for risk-seekers. The signal for risk and the signal for the value of risky reward covary with individual risk attitudes in regions of the human prefrontal cortex, suggesting subjective rather than objective coding of risk and risky value. These data demonstrate that important parameters of reward are coded in a subjective manner in key reward structures of the brain. However, these data do not rule out that other neurons or brain structures may code reward according to its objective value and risk. [source] CAC and routing for multi-service networks with blocked wide-band calls delayed, Part II: approximative link MDP frameworkEUROPEAN TRANSACTIONS ON TELECOMMUNICATIONS, Issue 1 2007Ernst Nordström In this paper, we study the call admission control (CAC) and routing issue in multi-service networks. Two categories of calls are considered: a narrow-band with blocked calls cleared and a wide-band with blocked calls delayed. The optimisation is subject to several quality of service (QoS) constraints, either on the packet or call level. The objective function is formulated as reward maximisation with penalty for delay. A suboptimal solution is achieved by applying Markov decision process (MDP) theory together with a three-level approximation. First, the network is decomposed into a set of links assumed to have independent Markov and reward processes respectively. Second, the dimensions of the link Markov and reward processes are reduced by aggregation of the call classes into call categories. Third, by applying decomposition of the link Markov process, the link MDP tasks are simplified considerably. The CAC and routing policy is computed by the policy iteration algorithm from MDP theory. The numerical results show that the proposed CAC and routing method, based on the approximate link MDP framework, is able to find an efficient trade-off between reward loss and average call set-up delay, outperforming conventional methods such as least loaded routing (LLR). Copyright © 2006 AEIT. [source] CAC and routing for multi-service networks with blocked wide-band calls delayed, part I: exact link MDP frameworkEUROPEAN TRANSACTIONS ON TELECOMMUNICATIONS, Issue 1 2006Ernst Nordström In this paper, we study the call admission control (CAC) and routing issue in multi-service networks. Two categories of calls are considered: a narrow-band (NB) with blocked calls cleared and a wide-band (WB) with blocked calls delayed. The objective function is formulated as reward maximisation with penalty for delay. The optimisation is subject to quality of service (QoS) constraints and, possibly, grade of service (GoS) constraints. A suboptimal solution is achieved by applying Markov decision process (MDP) theory together with a two-level approximation. First, the network is decomposed into a set of links assumed to have independent Markov and reward processes respectively. Second, the dimensions of the link Markov and reward processes are reduced by aggregation of the call classes into call categories. The CAC and routing policy is computed by the policy iteration algorithm from MDP theory. The numerical results show that the proposed CAC and routing method, based on the exact link MDP framework, is able to find an efficient trade-off between reward loss and average call set-up delay, outperforming conventional methods such as the least loaded routing (LLR). Copyright © 2005 AEIT. [source] Anandamide administration alone and after inhibition of fatty acid amide hydrolase (FAAH) increases dopamine levels in the nucleus accumbens shell in ratsJOURNAL OF NEUROCHEMISTRY, Issue 2 2006Marcello Solinas Abstract Although endogenous cannabinoid systems have been implicated in the modulation of the rewarding effects of abused drugs and food, little is known about the direct effects of endogenous ligands for cannabinoid receptors on brain reward processes. Here we show for the first time that the intravenous administration of anandamide, an endogenous ligand for cannabinoid receptors, and its longer-lasting synthetic analog methanandamide, increase the extracellular dopamine levels in the nucleus accumbens shell of awake, freely moving rats, an effect characteristic of most drugs abused by humans. Anandamide produced two distinctly different effects on dopamine levels: (1) a rapid, transient increase that was blocked by the cannabinoid CB1 receptor antagonist rimonabant, but not by the vanilloid VR1 receptor antagonist capsazepine, and was magnified and prolonged by the fatty acid amide hydrolase (FAAH) enzyme inhibitor, URB597; (2) a smaller delayed and long-lasting increase, not sensitive to CB1, VR1 or FAAH blockade. Both effects were blocked by infusing either tetrodotoxin (TTX, 1 µm) or calcium-free Ringer's solution through the microdialysis probe, demonstrating that they were dependent on the physiologic activation of dopaminergic neurotransmission. Thus, these results indicate that anandamide, through the activation of the mesolimbic dopaminergic system, participates in the signaling of brain reward processes. [source] Glutamate-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] The endocannabinoid system in brain reward processesBRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2008M Solinas Food, drugs and brain stimulation can serve as strong rewarding stimuli and are all believed to activate common brain circuits that evolved in mammals to favour fitness and survival. For decades, endogenous dopaminergic and opioid systems have been considered the most important systems in mediating brain reward processes. Recent evidence suggests that the endogenous cannabinoid (endocannabinoid) system also has an important role in signalling of rewarding events. First, CB1 receptors are found in brain areas involved in reward processes, such as the dopaminergic mesolimbic system. Second, activation of CB1 receptors by plant-derived, synthetic or endogenous CB1 receptor agonists stimulates dopaminergic neurotransmission, produces rewarding effects and increases rewarding effects of abused drugs and food. Third, pharmacological or genetic blockade of CB1 receptors prevents activation of dopaminergic neurotransmission by several addictive drugs and reduces rewarding effects of food and these drugs. Fourth, brain levels of the endocannabinoids anandamide and 2-arachidonoylglycerol are altered by activation of reward processes. However, the intrinsic activity of the endocannabinoid system does not appear to play a facilitatory role in brain stimulation reward and some evidence suggests it may even oppose it. The influence of the endocannabinoid system on brain reward processes may depend on the degree of activation of the different brain areas involved and might represent a mechanism for fine-tuning dopaminergic activity. Although involvement of the various components of the endocannabinoid system may differ depending on the type of rewarding event investigated, this system appears to play a major role in modulating reward processes. British Journal of Pharmacology (2008) 154, 369,383; doi:10.1038/bjp.2008.130; published online 14 April 2008 [source] | |||||||||||||