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PubMed2006

Phasic dopamine signaling during behavior, reward, and disease states.

The neurotransmitter dopamine is important in reward processing, however its precise modulatory role is still being investigated. Carbon-fiber microelectrodes can be used to monitor dopamine on a subsecond time scale in the striatum and nucleus accumbens of rats during behavior, and this approach is providing new insights into the mechanisms that control its extracellular concentration as well as the conditions under which it is released. Three main processes govern the amount of dopamine measured extrasynaptically: exocytotic release, neuronal uptake, and diffusion away from the release site. By monitoring local extracellular dopamine concentrations in the striatum following electrical stimulation of dopamine-containing neurons, release, uptake and diffusion can be individually examined and quantified. Dopaminergic neurons have been shown to fire in two firing modes, tonic and bursts at higher frequency. Electrical stimulation can be designed to mimic either mode to examine their effects on dopamine release. Burst firing causes a transient increase in extracellular dopamine while tonic firing causes a new steady-state level. In behaving primates, dopaminergic neurons display short-latency, phasic firing to primary reward and conditioned cues associated with reward. These bursts code differences between actual and predicted rewards. In rats, transient dopamine release in terminal regions that mimics that seen during burst firing has been demonstrated during reward-related cues. Taken together, these studies indicate that phasic dopamine release is a critical mediator of reward-related processes.

Action Potentials↗
PubMed2004

Integrating rewards and cognition in the frontal cortex.

Research indicates that the dorsolateral prefrontal cortex (DLPFC) contributes to working memory and executive control, whereas the ventral frontal cortex (VFC) contributes to affective and motivational processing. Few studies have examined both the functional specificity and the integration of these regions. We did so using fMRI and a verbal working memory task in which visual cues indicated whether recall performance on an upcoming trial would be linked to a monetary reward. On the basis of prior findings obtained in delayed response tasks performed by nonhuman primates, we hypothesized that (1) VFC would show an increase only in response to a cue indicating potential for a monetary reward; (2) DLPFC would show sustained activity across a delay interval for all trials, though activity in rewarded trials would be enhanced; and (3) regions engaged in speech-based rehearsal would be relatively insensitive to monetary incentive. Our hypotheses about DLPFC and rehearsal-related regions were confirmed. In VFC regions, we failed to observe statistically significant effects of reward when the cue or delay epochs of the task were examined in isolation. However, an unexpected and significant deactivation was observed in VFC during the delay epoch; furthermore, a post hoc voxelwise analysis indicated a complex interaction between (1) the cue and delay epochs of the task and (2) the reward value of the trials. The pattern of activation and deactivation across trial types suggests that VFC is sensitive to reward cues, and that portions of DLPFC and VFC may work in opposition during the delay epoch of a working memory task in order to facilitate task performance.

Adolescent↗
PubMed1987

[Interpersonal conflicts in reward allocation and their resolution].

Subjects performed a task in pairs and received false feedback concerning their performance levels. The performance level of one subject (HS) was set twice as high as the other (LS). It was predicted that (1) when the total rewards to be distributed between the two are dependent upon the sum of their performance scores, HS's and LS's equity judgments would agree with each other, but (2) when the total rewards are predetermined and not dependent upon their performance scores, HS would think that he/she deserves more than half of the rewards while LS would think that he/she deserves about half of the rewards. It was further predicted that the compromise between the two concerning reward distribution would be easier when accepting the partner's claim still yields referentially fair rewards to the subject than not. These predictions were supported in an experiment using 144 subjects in 72 same-sex pairs.

Conflict, Psychological↗
PubMed1999

Role of adenosine A2 receptors in brain stimulation reward under baseline conditions and during cocaine withdrawal in rats.

The present experiments tested the hypothesis that adenosine A2 receptors are involved in central reward function. Adenosine receptor agonists or antagonists were administered to animals that had been trained to self-stimulate in a rate-free brain stimulation reward (BSR) task that provides current thresholds as a measure of reward. The adenosine A(2A) receptor-selective agonists 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride (CGS 21680) (0.1-1.0 mg/kg) and 2-[(2-aminoethylamino)carbonylethyl phenylethylamino]-5'-N-ethylcarboxamido adenosine (APEC) (0.003-0.03 mg/kg) elevated reward thresholds without increasing response latencies, a measure of performance. Specifically, CGS 21680 had no effect on response latency, whereas APEC shortened latencies. Bilateral infusion of CGS 21680 (3, 10, and 30 ng/side), directly into the nucleus accumbens, elevated thresholds but shortened latencies. The highly selective A(2A) antagonist 8-(3-chlorostyryl)caffeine (0.01-10.0 mg/kg) and the A2-preferring antagonist 3,7-dimethyl-1-propargylxanthine (DMPX) (0.3-10.0 mg/kg) did not alter thresholds or latencies, but DMPX (1.0, 10.0 mg/kg) blocked the threshold-elevating effect of APEC (0.03 mg/kg). In another study, repeated administration of cocaine (eight cocaine injections of 15 mg/kg, i.p., administered over 9 hr) produced elevations in thresholds at 4, 8, and 12 hr after cocaine. DMPX (3 and 10 mg/kg), administered before both the 8 and 12 hr post-cocaine self-stimulation tests, reversed the threshold elevation produced by cocaine withdrawal. These results indicate that stimulating adenosine A(2A) receptors diminishes BSR without producing performance deficits, whereas blocking adenosine receptors reverses the reward impairment produced by cocaine withdrawal or by an A(2A) agonist. These findings indicate that adenosine, via A(2A) receptors, may inhibit central reward processes, particularly during the neuroadaptations associated with chronic drug-induced neuronal activation.

Adenosine↗
PubMed2000

NMDA, but not dopamine D(2), receptors in the rat nucleus accumbens areinvolved in guidance of instrumental behavior by stimuli predicting reward magnitude.

Expectancy of future reward is an important factor guiding the speed of instrumental behavior. The present study sought to explore whether signals transmitted via the NMDA subtype of glutamate receptors and via dopamine D(2) receptors in the nucleus accumbens (NAc) are critical for the determination of reaction times (RTs) of instrumental responses by the expectancy of future reward. A simple RT task for rats demanding conditioned lever release was used in which the upcoming reward magnitude (5 or 1 pellet) was signaled in advance by discriminative stimuli. In trained rats, RTs of conditioned responses with expectancy of a high reward magnitude were found to be significantly shorter. The shortening of RTs by stimuli predictive of high reward to be obtained was dose-dependently impaired by bilateral intra-NAc infusion of the competitive NMDA antagonist dl-2-amino-5-phosphonovaleric acid (APV) (1, 2, or 10 microg in 0.5 microl/side), but not by infusion of the preferential dopamine D(2) antagonist haloperidol (5 and 12.5 microg in 0.5 microl/side) or by infusion of vehicle (0.5 microl/side). In conclusion, the data reveal that in well trained animals stimulation of intra-NAc NMDA, but not of dopamine D(2), receptors, is critically involved in guiding the speed of instrumental responses according to stimuli predictive of the upcoming reward magnitude.

Animals↗
PubMed2001

Anticipation of increasing monetary reward selectively recruits nucleus accumbens.

Comparative studies have implicated the nucleus accumbens (NAcc) in the anticipation of incentives, but the relative responsiveness of this neural substrate during anticipation of rewards versus punishments remains unclear. Using event-related functional magnetic resonance imaging, we investigated whether the anticipation of increasing monetary rewards and punishments would increase NAcc blood oxygen level-dependent contrast (hereafter, "activation") in eight healthy volunteers. Whereas anticipation of increasing rewards elicited both increasing self-reported happiness and NAcc activation, anticipation of increasing punishment elicited neither. However, anticipation of both rewards and punishments activated a different striatal region (the medial caudate). At the highest reward level ($5.00), NAcc activation was correlated with individual differences in self-reported happiness elicited by the reward cues. These findings suggest that whereas other striatal areas may code for expected incentive magnitude, a region in the NAcc codes for expected positive incentive value.

Adult↗
PubMed2001

Incentive sensitization by previous amphetamine exposure: increased cue-triggered "wanting" for sucrose reward.

We reported previously that an amphetamine microinjection into the nucleus accumbens enables Pavlovian reward cues in a conditioned incentive paradigm to trigger excessive instrumental pursuit. Here we show that sensitization caused by previous amphetamine administration also causes reward cues to trigger excessive pursuit of their associated reward, even when sensitized rats are tested in a drug-free state. Rats learned to lever press for sucrose pellets, and they separately learned to associate sucrose pellets with Pavlovian cues (30 sec auditory cues). Amphetamine sensitization was induced by six daily injections of amphetamine (3 mg/kg, i.p.; controls received saline). Rats were tested for lever pressing under extinction conditions 10 d later, after a bilateral microinjection of intra-accumbens vehicle or amphetamine (5 microg/0.5 microl per side). Cue-triggered pursuit of sucrose reward was assessed by increases in pressing on the sucrose-associated lever during intermittent presentations of a free conditioned stimulus (CS+) sucrose cue. Sensitized rats pressed at normal levels during baseline and during the CS-, but the CS+ triggered 100% greater increases in pressing from sensitized rats than from control rats after vehicle microinjection. Sensitization therefore enhanced the incentive salience attributed to the CS+ even when rats were tested while drug-free. For control rats, a microinjection of intra-accumbens amphetamine was needed to produce the same enhancement of cue-triggered reward "wanting." The amphetamine microinjection also interacted synergistically in sensitized rats to produce intrusive cue-triggered pursuit behaviors (e.g., investigatory sniffing) that interfered with goal-directed lever pressing. These results support the incentive-sensitization theory postulate that sensitization causes excessive cue-triggered "wanting" for an associated reward.

Acoustic Stimulation↗
PubMed2002

Lesions of the tegmental pedunculopontine nucleus block the rewarding effects and reveal the aversive effects of nicotine in the ventral tegmental area.

Nicotine, the primary psychoactive component of tobacco smoke, is known to possess potent rewarding and aversive stimulus properties. The mammalian ventral tegmental area (VTA) is involved importantly in the mediation of the motivational effects of nicotine. However, the neural outputs from the VTA that may be involved in the transmission of the rewarding and aversive motivational effects of nicotine are not well understood. We report that bilateral lesions of the tegmental pedunculopontine nucleus (TPP) double dissociate the rewarding and aversive motivational effects of nicotine. Using a conditioned place preference paradigm, bilateral TPP lesions blocked a nicotine reward signal and revealed the aversive motivational properties of intra-VTA nicotine. These same TPP lesions did not block an aversive nicotine signal, as measured in a conditioned taste aversion paradigm. TPP lesions also produce an attenuation in nicotine-induced locomotor activity; however, neither learning nor performance deficits can account for these observed effects, because TPP-lesioned animals still showed clear aversive nicotine conditioning in two separate behavioral paradigms. Our results suggest that the rewarding effects of nicotine in the VTA are dependent on a nondopaminergic, descending reward pathway to the brainstem TPP.

Animals↗
PubMed2003

Selective disruption of stimulus-reward learning in glutamate receptor gria1 knock-out mice.

Glutamatergic neurotransmission via AMPA receptors has been an important focus of studies investigating neuronal plasticity. AMPA receptor glutamate receptor 1 (GluR1) subunits play a critical role in long-term potentiation (LTP). Because LTP is thought to be the cellular substrate for learning, we investigated whether mice lacking the GluR1 subunit [gria1 knock-outs (KO)] were capable of learning a simple cue-reward association, and whether such cues were able to influence motivated behavior. Both gria1 KO and wild-type mice learned to associate a light/tone stimulus with food delivery, as evidenced by their approaching the reward after presentation of the cue. During subsequent testing phases, gria1 KO mice also displayed normal approach to the cue in the absence of the reward (Pavlovian approach) and normal enhanced responding for the reward during cue presentations (Pavlovian to instrumental transfer). However, the cue did not act as a reward for learning a new behavior in the KO mice (conditioned reinforcement). This pattern of behavior is similar to that seen with lesions of the basolateral nucleus of the amygdala (BLA), and correspondingly, gria1 KO mice displayed impaired acquisition of responding under a second-order schedule. Thus, mice lacking the GluR1 receptor displayed a specific deficit in conditioned reward, suggesting that GluR1-containing AMPA receptors are important in the synaptic plasticity in the BLA that underlies conditioned reinforcement. Immunostaining for GluR2/3 subunits revealed changes in GluR2/3 expression in the gria1 KOs in the BLA but not the central nucleus of the amygdala (CA), consistent with the behavioral correlates of BLA but not CA function.

Acoustic Stimulation↗
PubMed2003

Hyperdopaminergic mutant mice have higher "wanting" but not "liking" for sweet rewards.

What is the role of dopamine in natural rewards? A genetic mutant approach was taken to examine the consequences of elevated synaptic dopamine on (1) spontaneous food and water intake, (2) incentive motivation and learning to obtain a palatable sweet reward in a runway task, and (3) affective "liking" reactions elicited by the taste of sucrose. A dopamine transporter (DAT) knockdown mutation that preserves only 10% of normal DAT, and therefore causes mutant mice to have 70% elevated levels of synaptic dopamine, was used to identify dopamine effects on food intake and reward. We found that hyperdopaminergic DAT knockdown mutant mice have higher food and water intake. In a runway task, they demonstrated enhanced acquisition and greater incentive performance for a sweet reward. Hyperdopaminergic mutant mice leave the start box more quickly than wild-type mice, require fewer trials to learn, pause less often in the runway, resist distractions better, and proceed more directly to the goal. Those observations suggest that hyperdopaminergic mutant mice attribute greater incentive salience ("wanting") to a sweet reward in the runway test. But sucrose taste fails to elicit higher orofacial "liking" reactions from mutant mice in an affective taste reactivity test. These results indicate that chronically elevated extracellular dopamine facilitates "wanting" and learning of an incentive motivation task for a sweet reward, but elevated dopamine does not increase "liking" reactions to the hedonic impact of sweet tastes.

Animals↗
PubMed1990

Dissociation of the attentional and motivational effects of pimozide on the threshold for rewarding brain stimulation.

The decreased sensitivity of animals to rewarding brain stimulation caused by pimozide has been interpreted as a selective pharmacologic blockade of central reward pathways rather than a nonspecific disruption of performance. In an attempt to confirm this hypothesis, the effects of pimozide on both reward and detection thresholds for intracranial stimulation delivered to the medial forebrain bundle-lateral hypothalamic area (MFB-LH) were determined in four animals. The drug caused a systematic increase in the reward threshold of each subject but had no such effect on the detection threshold. We conclude that pimozide selectively inhibits the rewarding effects of brain stimulation, and that therefore, the D2 dopamine receptor has a major role in activating central reward pathways subserving pharmacologic and electrical reinforcement. The dual anhedonic/antipsychotic effects of neuroleptic medication are discussed as a possible paradox of central importance to the psychopathology of schizophrenia.

Animals↗
PubMed1985

Probability-reward preferences of rhesus monkeys.

The relative preferences of rhesus monkeys for reward probability versus amount were investigated with procedures which contrasted general experience with specific instructions, and evaluated the relationship between probability-amount combinations and preference strength. Four stimulus objects, each signifying a different combination of reward frequency and amount (100% with one unit; 50% with two units; 33% with three units; or 25% with four units), were presented in pairs, one pair per daily session, with trial schedules providing the same amount of reward within each set of 12 trials. In Phase A, 4 monkeys (Group 1) were tested on the six choice-pairs with no preliminary training. In Phase B, Group 1 was joined by an additional 4 monkeys (Group 2), and each of the tasks was preceded by a demonstration of the relevant stimuli, one at a time, together with their associated probabilities and amounts. Group 1 animals developed preferences during Phase A for the more frequently rewarded objects, which persisted into Phase B, whereas Group 2 animals showed no preferences. This result indicates that preliminary instructions concerning the reward combinations associated with stimulus objects can prevent the development of a preference for greater probability over greater amount of reward, but cannot extinguish it once it has been formed or reestablished within the context of a particular task.

Animals↗
PubMed1996

Rewarding actions of phencyclidine and related drugs in nucleus accumbens shell and frontal cortex.

Rats learned to lever-press when such behavior was reinforced by microinjections of phencyclidine (PCP) directly into the ventromedial (shell) region of nucleus accumbens, indicating that the drug has direct rewarding actions in that region. Separate groups of rats learned to lever-press when reinforced with microinjections of dizoclipine (MK-801) or 3-((+/-)2-carboxypiperazin-4yl)propyl-1-phosphate (CPP), drugs known to block NMDA receptor function but not dopamine uptake, into the same region. Each drug was ineffective or markedly less effective when injected at a slightly more dorsal and lateral site in the core of nucleus accumbens. Self-administration of PCP, MK-801, or CPP directly into nucleus accumbens was not altered by co-infusion of a dose of the dopamine antagonist sulpiride that effectively blocked intracranial self-administration of the dopamine uptake inhibitor nomifensine, suggesting that the rewarding actions of the NMDA receptor antagonists are not dopamine-dependent. Rats also developed lever-pressing habits when PCP, MK-801, and CPP were each microinjected directly into frontal cortex, a region previously associated with the rewarding actions of cocaine but not nomifensine. Thus nucleus accumbens and frontal cortex are each potential substrates for the rewarding properties of PCP and related drugs, and the ability of these drugs to disrupt NMDA receptor function seems sufficient to account for their rewarding actions. When considered with independent evidence, the present results suggest a model of drug reward within which the critical event is inhibition of medium spiny neurons in nucleus accumbens.

Animals↗
PubMed1995

The D1 agonist SKF 38393 attenuates amphetamine-produced enhancement of responding for conditioned reward in rats.

The present study investigated the hypothesis that the D1 subtype of DA receptors is critically involved in reward-related learning. The effects of SKF 38393, a D1-specific agonist, on amphetamine-produced enhancement of responding for conditioned reward were tested. We exposed 69 male Wistar rats to an experimental design consisting of three phases. The preexposure phase consisted of five sessions during which the rats were exposed to an operant chamber containing two levers. One lever produced a lights-off stimulus (3 s) and the other a tone stimulus (3 s). This was followed by four conditioning sessions during which the levers were removed and the rats were exposed to pairings of the lights-off stimulus with food. This phase was followed by two test sessions during which the levers were present and the number of responses made on each lever was calculated as a ratio of the number of responses made during the preexposure phase. A group receiving saline during the test sessions showed a higher ratio of responding for the lights off stimulus than the tone stimulus, demonstrating that the lights-off stimulus had become a conditioned reward. Amphetamine [2.0 mg/kg, intraperitoneally (i.p.), 5 min before the test] enhanced responding specifically on the lever producing the conditioned reward. Groups receiving SKF 38393 (5.0, 10.0, and 20.0 mg/kg, i.p., 5 min before the test) failed to show significantly greater responding for the lights-off stimulus than the tone, indicating a reduction or elimination of the conditioned reward effect. Moreover, SKF 38393 dose dependently reduced the amphetamine-produced enhancement of responding for conditioned reward.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2004

Effect of aging on stimulus-reward association learning.

The flexible learning of stimulus-reward associations when required by situational context is essential for everyday behavior. Older adults experience a progressive decline in several cognitive functions and show deficiencies in neuropsychological tasks requiring flexible adaptation to external feedback, which could be related to impairments in reward association learning. To study the effect of aging on stimulus-reward association learning 20 young and 20 older adults performed a probabilistic object reversal task (pORT) along with a battery of tests assessing executive functions and general intellectual abilities. The pORT requires learning and reversing associations between actions and their outcomes. Older participants collected fewer points, needed more trials to reach the learning criterion, and completed less blocks successfully compared to young adults. This difference remained statistically significant after correcting for the age effect of other tests assessing executive functions. This suggests that there is an age-related difference in reward association learning as measured using the pORT, which is not closely related to other executive functions with respect to the age effect. In human aging, structural alterations of reward detecting structures and functional changes of the dopaminergic as well as the serotonergic system might contribute to the deficit in reward association learning observed in this study.

Adult↗
PubMed1991

Characteristics of spatiotemporal integration in the priming and rewarding effects of medial forebrain bundle stimulation.

Only the function relating the required pulse frequency to the interburst interval discriminates between the priming effect and the rewarding effect: Separating two short bursts of pulses has no effect on their combined rewarding effect, but it enhances their priming effect. There are significant nonscalar differences between animals in the number-current and charge-duration functions for priming and reward, but there are no significant differences in these functions between effects within animals. Substantially more electrical-stimulation is required to produce good priming than to produce a reward that sustains maximum possible levels of performance. These findings suggest that the priming effect is a transient excitement generated by the receipt of one or more very large rewards. The discussion elaborates a model that reconciles this hypothesis with the earlier finding that the rewarding effect may be blocked pharmacologically without blocking priming.

Animals↗
PubMed2004

Control of variation by reward probability.

Two bar-press experiments with rats tested the rule that reducing expectation of reward increases the variation from which reward selects. Experiment 1 used a discrete-trial random-interval schedule, with trials signaled by light or sound. One signal always ended with reward; the other signal ended with reward less often. The 2 signals were randomly mixed. Bar-press duration (how long the bar was held down) varied more during the signal with the lower probability of reward. Experiment 2 closely resembled Experiment 1 but used a random-ratio schedule rather than a random-interval schedule. Again, bar-press duration varied more during the signal with the lower probability of reward. The results support the rule--the first well-controlled comparisons to do so.

Animals↗
PubMed2001

Different effort constructs and effort-reward imbalance: effects on employee well-being in ancillary health care workers.

AIMS OF THE STUDY: The present study investigates the relationship between Effort-Reward Imbalance (ERI) and employee well-being, using three different concepts of efforts (i.e. psychological demands, physical demands and emotional demands). BACKGROUND: The ERI model had been used as a theoretical framework, indicating that work stress is related to high efforts (i.e. job demands) and low occupational rewards (e.g. money, esteem and security/career opportunities). The ERI model also predicts that, in overcommitted workers, effects of ERI on employee well-being are stronger compared with their less committed counterparts. METHODS: A cross-sectional survey among 167 ancillary health care workers of two nursing homes was conducted. Multiple univariate logistic regression analyses were used to test the relationship between ERI and employee well-being. RESULTS: Results of the logistic regression analyses showed that employees with both high (psychological, physical and emotional) efforts and low rewards had higher risks of psychosomatic health complaints, physical health symptoms and job dissatisfaction (odds ratios (ORs) ranged from 5.09 to 18.55). Moreover, employees who reported both high efforts and high rewards had elevated risks of physical symptoms and exhaustion (ORs ranged from 6.17 to 9.39). No support was found for the hypothesis on the moderating effect of overcommitment. CONCLUSION: Results show some support for the ERI model; ancillary health care workers with high effort/low reward imbalance had elevated risks of poor employee well-being. In addition, results show that the combination of high efforts and high rewards is important for employee well-being. Finally, some practical implications are discussed to combat work stress in health care work.

Adolescent↗