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At least 433 records · Page 24Linked to original sources
PubMed2006

Visual selective attention and the effects of monetary rewards.

Outcomes of actions, in the form of rewards and punishments, are known to shape behavior. For example, an action followed by reward will be more readily elicited on subsequent encounters with the same stimuli and context -- a phenomenon known as the law of effect. These consequences of rewards (and punishments) are important because they reinforce adaptive behaviors at the expense of competing ones, thus increasing fitness of the organism in its environment. However, it is unknown whether similar influences regulate covert mental processes, such as visual selective attention. Visual selective attention allows privileged processing of task-relevant information, while inhibiting distracting contextual elements. Using variable monetary rewards as arbitrary feedback on performance, we tested whether acts of attentional selection, and in particular the resulting aftereffects, can be modulated by their consequences. Results show that the efficacy of visual selective attention can be sensibly adjusted by external feedback. Specifically, although lingering inhibition of distractors is robust after highly rewarded selections, it is eliminated after poorly rewarded selections. This powerful feature of visual selective attention provides attentive processes with both flexibility and self-regulation properties.

Adult↗
PubMed2006

ADHD and delay aversion: the influence of non-temporal stimulation on choice for delayed rewards.

BACKGROUND: Delay aversion, the motivation to escape or avoid delay, results in preference for small immediate over large delayed rewards. Delay aversion has been proposed as one distinctive psychological process that may underlie the behavioural symptoms and cognitive deficits of attention deficit/hyperactivity disorder (ADHD). Furthermore, the delay aversion hypothesis predicts that ADHD children's preference for immediate small over large delayed rewards will be reduced when stimulation, which makes time appear to pass more quickly, is added to the delay interval. The current paper tests these predictions. METHODS: A group of children with a diagnosis of ADHD (with or without oppositional defiant disorder (ODD)), a group with a diagnosis of high-functioning autism (HFA), and a normal control group were compared on an experimental paradigm giving repeated choices between small immediate and large delayed rewards (Maudsley Index of Delay Aversion-MIDA) under two conditions (stimulation and no stimulation). RESULTS: As predicted, ADHD children displayed a stronger preference than the HFA and control children for the small immediate rewards under the no-stimulation condition. The ADHD children preferences were normalised under the stimulation condition with no differences between the groups. This pattern of results was the same whether the ADHD children had comorbid ODD or not. DISCUSSION: The findings from the MIDA are consistent with the delay aversion hypothesis of ADHD in showing that preference for small immediate rewards over large delayed rewards is a specific feature of ADHD and that this preference can be reduced by the addition of stimulation. Further research is required to better understand the emotional and motivational mechanisms underpinning delay aversion.

Adolescent↗
PubMed2005

The role of dopamine in reward and pleasure behaviour--review of data from preclinical research.

OBJECTIVE: The purpose of this article is to review some of the basic aspects of the dopaminergic system and its role in reward and pleasure behaviour. We also discuss the association between dopamine and unpleasant symptoms that are commonly found in neuropsychiatric disorders and may also be side-effects of neuroleptic drugs. METHOD: A computer-based search of the literature, augmented by extensive bibliography-guided article reviews, were used to find basic information on the dopamine and the reward systems, and symptoms such as dysphoria, anhedonia and depression. RESULTS: Central dopaminergic neurotransmission is complex, having multiple actions at each level of the mesocorticolimbic reward pathway. The role of dopamine in the reward process was classically associated with the ability to experience pleasure; recent data suggest a more motivational role. Dysfunction of the dopamine transmission in the reward circuit is associated with symptoms such as anhedonia, apathy and dysphoria found in several neuropsychiatric disorders, including Parkinson's disease, depression, drug addiction, and neuroleptic-induced dysphoria. CONCLUSION: Viewing the dysfunctions of the reward pathways within a broader spectrum and exploring its complex relations with the dopaminergic transmission may help understand the pathophysiology of these neuropsychiatric disorders and lead to a rational development of novel treatments.

Affect↗
PubMed2003

Group II metabotropic and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainate glutamate receptors regulate the deficit in brain reward function associated with nicotine withdrawal in rats.

This study investigated the role of ionotropic and metabotropic glutamate receptors in the deficits in brain reward function, as measured by elevations in intracranial self-stimulation (ICSS) reward thresholds, associated with nicotine withdrawal. The group II metabotropic glutamate (mGluII) receptor agonist LY314582 [a racemic mixture of LY354740 ([+]-2-aminobicyclo[3.1.0]hexane-2,6-dicarboxylic acid])] (2.5-7.5 mg/kg) precipitated withdrawal-like elevations in ICSS thresholds, a sensitive measure of reward function, in nicotine-dependent but not control rats. LY314582 did not affect response latencies, a measure of performance in the ICSS paradigm. Bilateral microinfusion of LY314582 (10-100 ng/side) into the ventral tegmental area likewise precipitated dose-dependent threshold elevations in nicotine-dependent rats. Furthermore, a single injection of the mGluII receptor antagonist LY341495 (2S-2-amino-2-[1S,2S-2-carboxycyclopropan-1-yl]-3-[xanth-9-yl]propionic acid) (1 mg/kg) attenuated the threshold elevations observed in rats undergoing spontaneous nicotine withdrawal. mGluII receptors are primarily located on glutamatergic terminals throughout the mesocorticolimbic system, where they act as inhibitory autoreceptors. To investigate whether mGluII receptors contributed to nicotine withdrawal by decreasing glutamatergic transmission, we next examined whether direct blockade of postsynaptic glutamate receptors precipitated withdrawal-like reward deficits in nicotine-dependent rats. The alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainate receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX; 0.01-1 mg/kg) precipitated withdrawal-like threshold elevations in nicotine-dependent but not control rats, whereas 6-methyl-2-[phenylethynyl]-pyridine (MPEP; 0.01-3 mg/kg) and dizocilpine (MK-801; 0.01-0.2 mg/kg), antagonists at metabotropic glutamate 5 and N-methyl-d-aspartate receptors, respectively, did not. Overall, these data demonstrate that mGluII receptors play an important role in the reward deficits associated with nicotine withdrawal. Furthermore, it is likely that mGluII receptors generate this reward deficit, at least in part, by decreasing glutamate transmission at AMPA/kainate receptors.

Animals↗
PubMed2002

Anterior cingulate: single neuronal signals related to degree of reward expectancy.

As monkeys perform schedules containing several trials with a visual cue indicating reward proximity, their error rates decrease as the number of remaining trials decreases, suggesting that their motivation and/or reward expectancy increases as the reward approaches. About one-third of single neurons recorded in the anterior cingulate cortex of monkeys during these reward schedules had responses that progressively changed strength with reward expectancy, an effect that disappeared when the cue was random. Alterations of this progression could be the basis for the changes from normal that are reported in anterior cingulate population activity for obsessive-compulsive disorder and drug abuse, conditions characterized by disturbances in reward expectancy.

Action Potentials↗
PubMed1967

Reward and learning in the goldfish.

An experiment with goldfish showed the effects of change in amount of reward that are predicted from reinforcement theory. The performance of animals shifted from small to large reward improved gradually to the level of unshifted large-reward controls, while the performance of animals shifted from large to small reward remained at the large-reward level. The difference between these results and those obtained in analogous experiments with the rat suggests that reward functions differently in the instrumental learning of the two animals.

Animals↗
PubMed2006

Behavioral theories and the neurophysiology of reward.

The functions of rewards are based primarily on their effects on behavior and are less directly governed by the physics and chemistry of input events as in sensory systems. Therefore, the investigation of neural mechanisms underlying reward functions requires behavioral theories that can conceptualize the different effects of rewards on behavior. The scientific investigation of behavioral processes by animal learning theory and economic utility theory has produced a theoretical framework that can help to elucidate the neural correlates for reward functions in learning, goal-directed approach behavior, and decision making under uncertainty. Individual neurons can be studied in the reward systems of the brain, including dopamine neurons, orbitofrontal cortex, and striatum. The neural activity can be related to basic theoretical terms of reward and uncertainty, such as contiguity, contingency, prediction error, magnitude, probability, expected value, and variance.

Animals↗
PubMed2002

Reward-dependent spatial selectivity of anticipatory activity in monkey caudate neurons.

Many neurons show anticipatory activity in learned tasks. This phenomenon appears to reflect the brain's ability to predict future events. However, what actually is predicted is unknown. Using a memory-guided saccade task, in which only one out of four directions was rewarded in each block of trials, we found that a group of neurons in the monkey caudate nucleus (CD) showed activity before presentation of an instruction cue stimulus. Among 329 CD neurons that were related to memory-guided saccade tasks, 156 showed the precue activity and 91 of them were examined fully. Remarkably, the magnitude of the precue activity varied across the four blocks of the one-direction-rewarded (1DR) condition, depending on which direction was rewarded. A majority of neurons with precue activity (83/91, 91%) showed significant directional preference. The best and worst directions were usually in the contralateral and ipsilateral directions, respectively. Within a block, the precue activity increased rapidly for the best direction in 1DR and decreased gradually for the worst direction in 1DR and all-directions-rewarded (ADR) condition. The precue activity was weak in ADR. The precue activity did not reflect the likelihood of a particular cue stimulus, because the probability of the cue appearing in each direction was the same regardless of the rewarded direction. These results suggest that each CD neuron indicates a particular position-reward association prospectively, usually with contralateral preference. Assuming that the CD neurons have access to saccadic motor outputs, the precue activity would create a motivational bias toward the contralateral space, even before an instruction is given by the cue stimulus.

Acoustic Stimulation↗
PubMed2003

The anterior cingulate and reward-guided selection of actions.

Macaques were taught a reward-conditional response selection task; they learned to associate each of two different actions to each of two different rewards and to select actions that were appropriate for particular rewards. They were also taught a visual discrimination learning task. Cingulate lesions significantly impaired selection of responses associated with different rewards but did not interfere with visual discrimination learning or performance. The results suggest that 1) the cingulate cortex is concerned with action reward associations and not limited to just detecting when actions lead to errors and 2) that the cingulate cortex's function is limited to action reinforcer associations and it is not concerned with stimulus reward associations.

Animals↗
PubMed2005

Human neural learning depends on reward prediction errors in the blocking paradigm.

Learning occurs when an outcome deviates from expectation (prediction error). According to formal learning theory, the defining paradigm demonstrating the role of prediction errors in learning is the blocking test. Here, a novel stimulus is blocked from learning when it is associated with a fully predicted outcome, presumably because the occurrence of the outcome fails to produce a prediction error. We investigated the role of prediction errors in human reward-directed learning using a blocking paradigm and measured brain activation with functional magnetic resonance imaging. Participants showed blocking of behavioral learning with juice rewards as predicted by learning theory. The medial orbitofrontal cortex and the ventral putamen showed significantly lower responses to blocked, compared with nonblocked, reward-predicting stimuli. In reward-predicting control situations, deactivation in orbitofrontal cortex and ventral putamen occurred at the time of unpredicted reward omissions. Responses in discrete parts of orbitofrontal cortex correlated with the degree of behavioral learning during, and after, the learning phase. These data suggest that learning in primary reward structures in the human brain correlates with prediction errors in a manner that complies with principles of formal learning theory.

Adult↗
PubMed2006

Effort-reward imbalance at work and the co-occurrence of lifestyle risk factors: cross-sectional survey in a sample of 36,127 public sector employees.

BACKGROUND: In occupational life, a mismatch between high expenditure of effort and receiving few rewards may promote the co-occurrence of lifestyle risk factors, however, there is insufficient evidence to support or refute this hypothesis. The aim of this study is to examine the extent to which the dimensions of the Effort-Reward Imbalance (ERI) model--effort, rewards and ERI--are associated with the co-occurrence of lifestyle risk factors. METHODS: Based on data from the Finnish Public Sector Study, cross-sectional analyses were performed for 28,894 women and 7233 men. ERI was conceptualized as a ratio of effort and rewards. To control for individual differences in response styles, such as a personal disposition to answer negatively to questionnaires, occupational and organizational-level ecological ERI scores were constructed in addition to individual-level ERI scores. Risk factors included current smoking, heavy drinking, body mass index > or =25 kg/m2, and physical inactivity. Multinomial logistic regression models were used to estimate the likelihood of having one risk factor, two risk factors, and three or four risk factors. The associations between ERI and single risk factors were explored using binary logistic regression models. RESULTS: After adjustment for age, socioeconomic position, marital status, and type of job contract, women and men with high ecological ERI were 40% more likely to have simultaneously > or =3 lifestyle risk factors (vs. 0 risk factors) compared with their counterparts with low ERI. When examined separately, both low ecological effort and low ecological rewards were also associated with an elevated prevalence of risk factor co-occurrence. The results obtained with the individual-level scores were in the same direction. The associations of ecological ERI with single risk factors were generally less marked than the associations with the co-occurrence of risk factors. CONCLUSION: This study suggests that a high ratio of occupational efforts relative to rewards may be associated with an elevated risk of having multiple lifestyle risk factors. However, an unexpected association between low effort and a higher likelihood of risk factor co-occurrence as well as the absence of data on overcommitment (and thereby a lack of full test of the ERI model) warrant caution in regard to the extent to which the entire ERI model is supported by our evidence.

Adolescent↗
PubMed2004

Molecular mechanisms underlying the rewarding effects of cocaine.

The initially surprising observation that cocaine retains its rewarding effects in dopamine transporter (DAT) knockout (KO) mice led our laboratory to examine the effects of deletion of other monoaminergic genes on cocaine reward. Our initial approach to this problem was to combine DAT KO mice with serotonin transporter (SERT) KO mice to make combined DAT/SERT KO mice. The combination of these knockouts eliminates cocaine reward as assessed in the conditioned place preference (CPP) paradigm. We have also identified evidence that, in the absence of DAT, there is greater participation in cocaine reward by serotonin (SERT) and norepinephrine (NET) transporters. Both NET and SERT blockers (nisoxetine and fluoxetine) produced significant CPPs in DAT KO mice, but not in wild-type (WT) mice. The striking elimination of cocaine CPP in combined DAT/SERT KO mice contrasts with effects that we have identified in combined NET/SERT knockout mice, which display increases in cocaine reward, and with recent reports that suggest that DAT/NET combined KOs retain substantial cocaine CPP. Overall, these studies indicate important requirements for several monoaminergic system genes to fully explain cocaine reward, in particular those expressed by dopamine and serotonin systems.

Animals↗
PubMed2006

Reward-related cortical inputs define a large striatal region in primates that interface with associative cortical connections, providing a substrate for incentive-based learning.

The anterior cingulate and orbital cortices and the ventral striatum process different aspects of reward evaluation, whereas the dorsolateral prefrontal cortex and the dorsal striatum are involved in cognitive function. Collectively, these areas are critical to decision making. We mapped the striatal area that receives information about reward evaluation. We also explored the extent to which terminals from reward-related cortical areas converge in the striatum with those from cognitive regions. Using three-dimensional-rendered reconstructions of corticostriatal projection fields along with two-dimensional chartings, we demonstrate the reward and cognitive territories in the primate striatum and show the convergence between these cortical inputs. The results show two labeling patterns: a focal projection field that consists of densely distributed terminal patches, and a diffuse projection consisting of clusters of fibers, extending throughout a wide area of the striatum. Together, these projection fields demonstrate a remarkably large, rostral, reward-related striatal territory that reaches into the dorsal striatum. Fibers from different reward-processing and cognitive cortical areas occupy both separate and converging territories. Furthermore, the diffuse projection may serve a separate integrative function by broadly disseminating general cortical activity. These findings show that the rostral striatum is in a unique position to mediate different aspects of incentive learning. Furthermore, areas of convergence may be particularly sensitive to dopamine modulation during decision making and habit formation.

Animals↗
PubMed2005

Regulation of drug reward by cAMP response element-binding protein: evidence for two functionally distinct subregions of the ventral tegmental area.

The transcription factor cAMP response element binding protein (CREB) is implicated in the actions of drugs of abuse in several brain areas, but little information is available about a role for CREB in the ventral tegmental area (VTA), one of the key reward regions of the brain. Here, we demonstrate that chronic exposure to drugs of abuse induces CREB activity throughout the VTA. Using viral-mediated gene transfer, we expressed green fluorescent protein (GFP)-tagged CREB or mCREB (a dominant-negative form of CREB) in the VTA and, using a conditioned place-preference paradigm, found that CREB activation within the rostral versus caudal subregions of the VTA produces opposite effects on drug reward. We identified VTA subregion-specific differences in the proportion of dopaminergic and GABAergic neurons and in the dopaminergic projections to the nucleus accumbens, another brain region implicated in drug reward, and suggest that this may contribute to behavioral differences in this study. We also measured expression levels of tyrosine hydroxylase and the AMPA glutamate receptor subunit GluR1, both of which are known to contribute to drug reward in the VTA, and found that both of these genes are upregulated following the expression of CREB-GFP and downregulated following expression of mCREB-GFP, raising the possibility that CREB may exert its effects on drug reward, in part, via regulation of these genes. These results suggest a novel role for CREB in mediating drug-induced plasticity in the VTA and establish two functionally distinct subregions of the VTA in which CREB differentially regulates drug reward.

Animals↗
PubMed2006

Conditioned withdrawal drives heroin consumption and decreases reward sensitivity.

Aspects of drug withdrawal may become conditioned to previously neutral environmental stimuli via classical conditioning processes. Nevertheless, the significance of conditioned withdrawal effects in motivating drug intake remains largely unexplored. Here, we investigated the effects of conditioned withdrawal in modulating heroin consumption and brain reward sensitivity in rats. Rats intravenously self-administered heroin (20 microg/infusion) during 0 h (control), 1 h (nondependent), or 23 h (dependent) sessions and had daily intracranial self-stimulation (ICSS) thresholds assessed. ICSS thresholds remained stable and unaltered in control rats. In nondependent rats, heroin self-administration induced a transient activation of reward systems, reflected in lowering of ICSS thresholds. In dependent rats, heroin intake escalated across sessions and was associated with a gradual decrease in reward sensitivity, reflected in progressively elevated ICSS thresholds. Thus, as dependence develops, heroin may be consumed not only for its acute reward-facilitating effects, but also to counter persistent deficits in reward sensitivity. In nondependent rats, the opioid receptor antagonist naloxone (30 microg/kg) increased heroin consumption and reversed heroin-induced lowering of ICSS thresholds, effects resistant to classical conditioning. In contrast, in dependent rats naloxone (30 microg/kg) increased heroin consumption and also elevated ICSS thresholds above their already elevated baseline levels (i.e., precipitated withdrawal). Most importantly, stimuli repeatedly paired with naloxone-precipitated withdrawal provoked heroin consumption and elevated ICSS thresholds in dependent rats. Thus, conditioned stimuli predicting the onset of heroin withdrawal, and hence the reward deficits coupled with this state, may play a critical role in provoking craving and relapse in human opiate addicts.

Animals↗
PubMed2004

A neural correlate of reward-based behavioral learning in caudate nucleus: a functional magnetic resonance imaging study of a stochastic decision task.

Humans can acquire appropriate behaviors that maximize rewards on a trial-and-error basis. Recent electrophysiological and imaging studies have demonstrated that neural activity in the midbrain and ventral striatum encodes the error of reward prediction. However, it is yet to be examined whether the striatum is the main locus of reward-based behavioral learning. To address this, we conducted functional magnetic resonance imaging (fMRI) of a stochastic decision task involving monetary rewards, in which subjects had to learn behaviors involving different task difficulties that were controlled by probability. We performed a correlation analysis of fMRI data by using the explanatory variables derived from subject behaviors. We found that activity in the caudate nucleus was correlated with short-term reward and, furthermore, paralleled the magnitude of a subject's behavioral change during learning. In addition, we confirmed that this parallelism between learning and activity in the caudate nucleus is robustly maintained even when we vary task difficulty by controlling the probability. These findings suggest that the caudate nucleus is one of the main loci for reward-based behavioral learning.

Adult↗
PubMed2004

Independent coding of reward magnitude and valence in the human brain.

Previous research has shown that two components of the event-related brain potential, the P300 and feedback negativity, are sensitive to information about rewards and penalties. The present study investigated the properties of these components in a simple gambling game that required participants to choose between cards that were unpredictably associated with monetary gains and losses of variable magnitude. The aim was to determine the sensitivity of each component to two critical features of reward stimuli: magnitude (small or large) and valence (win or loss). A double dissociation was observed, with the P300 sensitive to reward magnitude but insensitive to reward valence and the feedback negativity showing the opposite pattern, suggesting that these two fundamental features of rewarding stimuli are evaluated rapidly and separately in the human brain. Subsequent analyses provided additional evidence of functional dissociations between the feedback negativity and P300. First, the P300 (but not the feedback negativity) showed sensitivity to the reward value of alternative, nonselected stimuli. Second, individual differences in the amplitude of the feedback negativity correlated with individual differences in risk-taking behavior observed after monetary losses, whereas individual differences in P300 amplitude were related to behavioral adjustments observed in response to alternative, unchosen outcomes.

Adolescent↗
PubMed2004

Rewarding effects of AMPA administration into the supramammillary or posterior hypothalamic nuclei but not the ventral tegmental area.

We examined whether injections of the excitatory amino acid AMPA are rewarding when injected into the posterior hypothalamus and ventral tegmental area. Rats quickly learned to lever-press for infusions of AMPA into the supramammillary or posterior hypothalamic nuclei but failed to learn to lever-press for similar injections into the ventral tegmental areas. AMPA injections into the supramammillary nucleus, but not the ventral tegmental area, induced conditioned place preference. The rewarding effects of AMPA appear to be mediated by AMPA receptors, because coadministration of the AMPA antagonist CNQX blocked the rewarding effects of AMPA, and administration of the enantiomer R-AMPA did not mimic the rewarding effects. AMPA injections into the supramammillary nucleus, but not the ventral tegmental area, also increased extracellular dopamine concentrations in the nucleus accumbens. Pretreatment with the D1 dopamine antagonist SCH 23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine] led to extinction of AMPA self-administration. These findings implicate posterior hypothalamic regions in reward function and suggest that reward mechanisms localized around the ventral tegmental area are more complex than has been assumed recently.

Animals↗