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PubMed2006

Question-based assessments of delay discounting: do respondents spontaneously incorporate uncertainty into their valuations for delayed rewards?

This research was designed to determine if, and to what extent, participants incorporate uncertainty into their valuations for delayed rewards when completing measures of delay discounting, even though uncertainty is not specified in the delay-discounting questions. Twenty-four adolescent participants completed a question-based measure of delay discounting and immediately following answered questions about perceived certainties of receiving the delayed rewards. Results showed that respondents rated the delayed rewards as increasingly uncertain with longer delays. Also, ratings of uncertainty were correlated with rate of delay discounting (r=0.55). These findings suggest participants automatically evaluate delayed rewards as uncertain when using this assessment procedure. The current finding may hold important implications for future addiction research in interpreting why addicted persons often discount more by delay than non-addicted controls, i.e., delay to reward or uncertainty about delayed rewards?

Adolescent↗
PubMed2006

Brain reward deficits accompany withdrawal (hangover) from acute ethanol in rats.

Withdrawal from an acute bolus injection of ethanol produces affective or emotional signs that include anxiogenic-like behavior and conditioned place aversion. This study assessed whether brain reward deficits that accompany withdrawal from chronic ethanol dependence are also observed upon withdrawal from acute intoxication. Rats were implanted with stimulating electrodes aimed at the medial forebrain bundle in the lateral hypothalamus and trained on a discrete-trial current-intensity brain stimulation reward threshold paradigm. Ethanol intoxication was produced by bolus intraperitoneal injections of ethanol (1.0, 1.5, or 2.0 g/kg). Brain reward thresholds were monitored periodically following the bolus injection (3, 6, 9, 12, 24, 48, 72, 96 h postethanol). Blood samples taken at various intervals postethanol revealed that peak blood alcohol levels (BAL) at all doses tested were reached within 10 min of injection. Following doses of 1.0, 1.5, and 2.0 g/kg ethanol, BAL had declined to undetectable levels within 3-6h postinjection. Withdrawal from a single injection of ethanol resulted in a significant but transient increase in brain reward thresholds only with the highest ethanol dose tested (2.0 g/kg). When acute intoxication and withdrawal episodes were repeated two additional times at weekly intervals, the peak magnitude and duration of threshold elevation increased significantly at the 2.0 g/kg dose of ethanol. A significant but transient increase in thresholds was also seen in the group treated with 1.5 g/kg ethanol during the third and final week of testing. Results indicate that withdrawal from a single exposure to an intoxicating dose of ethanol produces significant brain reward deficits in addition to other affective disturbances previously reported, and that repeated weekly intoxication and withdrawal results in a progressive increase in magnitude and duration of the reward deficit.

Affective Symptoms↗
PubMed2004

Sensitivity to reward: implications for overeating and overweight.

Sensitivity to reward (STR)-a personality trait firmly rooted in the neurobiology of the mesolimbic dopamine system-has been strongly implicated in the risk for addiction. This construct describes the ability to derive pleasure or reward from natural reinforcers like food, and from pharmacologic rewards like addictive drugs. Recently experts in the field of addiction research have acknowledged that psychomotor stimulant drugs are no longer at the heart of all addictions, and that brain circuits can also be deranged with natural rewards like food. The present study tested a model in which STR was expected to relate positively to overeating, which in turn would be associated with higher body weight in woman aged 25-45 years. As predicted, STR was correlated positively with measures of emotional overeating. Also, overweight woman were significantly more sensitive to reward than those of normal weight. Interestingly, however, the obese woman (Body Mass Index>30) were more anhedonic than the overweight woman (Body Mass Index>25<30). These findings are discussed in the context of neuroadaptations to overactivity of brain reward circuits. Results also indicate that STR may serve as a risk factor for overeating and overweight, especially in cultures such as ours where palatable, calorically-dense food is plentiful.

Adult↗
PubMed2004

Differential reward outcome learning in adult humans.

Differential reward outcome learning provides a unique reward outcome for each condition of a conditional discrimination task, and this increases the rate at which these tasks can be learned. The present experiment aims to show that irrespective of any difference in learning rate, conditional discrimination tasks and differential reward outcome tasks are solved using different strategies. Two groups of 30 adult subjects were taught a series of conditional visual discriminations. One group received different reward outcomes for each condition, whilst the other group received the same reward outcome for each condition. Both groups learned the visual discriminations at the same rate. Subjects were then taught a new conditional cue with a subset of previously learnt discrimination problems and then required to transfer the newly learnt instruction cue to the remaining discrimination problems that had been previously learnt. Although both groups appeared to transfer the newly learnt cue at the same rate, the subjects performing the differential reward outcome task learnt to a criterion level of performance with fewer errors. The results are discussed in relation to evidence from monkeys indicating different neural mechanisms underlying the learning of both tasks.

Adolescent↗
PubMed2005

Alterations in morphine-induced reward, locomotor activity, and thermoregulation in CREB-deficient mice.

Previous studies in our lab have shown a robust decrease in the rewarding properties of morphine in CREB(alphaDelta) mutant mice. To determine whether the genetic effects of the global CREB(alphaDelta) mutation are specific to reward or generalizable, we examined a variety of morphine-induced behaviors regulated by different neural circuitry. At low doses of morphine (5 and 10 mg/kg), CREB(alphaDelta) mutant mice show a reduction in reward yet similar locomotor activity in response to morphine compared to wild type littermates. However, at a high dose (20 mg/kg), CREB(alphaDelta) mutant mice show an increase in reward and locomotor activity. Morphine-induced thermoregulation is attenuated in CREB(alphaDelta) mutant mice at high doses of morphine compared to wild type animals. The behavioral differences in response to morphine seen in CREB(alphaDelta) mutant mice are not due to changes in mu opioid receptor (MOR) mRNA expression, as the CREB deletion has no effect on baseline MOR mRNA in three of the brain regions involved in mediating these behaviors: the ventral tegmental area (VTA), nucleus accumbens (NAc), and hypothalamus. These data demonstrate that at low doses, deficits in morphine-induced changes in CREB deficient mice are limited to reward and thermoregulation. However, at higher doses, CREB mutant mice actually find morphine more rewarding and exhibit increased locomotor activity compared to their wild type littermates. Together, these results indicate that the role of CREB in dose-dependent changes in behaviors induced by morphine is different depending on the brain regions involved in mediating the behavior.

Analysis of Variance↗
PubMed2005

Decreased sensitivity to the effects of dopamine D1-like, but not D2-like, receptor antagonism in the posterior hypothalamic region/anterior ventral tegmental area on brain reward function during chronic exposure to nicotine in rats.

Chronic administration of nicotine induces adaptations in central nervous system function to counteract nicotine's acute effects. When nicotine administration ceases, these adaptations remain unopposed and may lead to drug withdrawal. The present studies were conducted to assess the effects of chronic nicotine administration on dopamine D1- and D2-like receptor activity in the posterior hypothalamus/anterior ventral tegmental area (VTA). An intracranial self-stimulation discrete trial procedure that provides current intensity thresholds was used to provide a measure of brain reward function in rats. Previous studies showed that systemic administration of dopamine D1- or D2-like receptor antagonists induced elevations in brain reward thresholds in drug-free rats, indicative of a decrease in brain reward function. We show here that injections of the D1-like receptor antagonist SCH 23390 (1-4 microg total bilateral dose) into the posterior hypothalamus/anterior VTA differentially elevated brain reward thresholds in rats chronically treated with nicotine (9 mg/kg/day, salt) versus saline-treated rats. The nicotine-treated rats were less sensitive to the threshold elevating effects of D1-like receptor antagonism. By contrast, the D2-like receptor antagonist eticlopride (1-4 microg total bilateral dose) injected into the posterior hypothalamus/anterior VTA significantly elevated brain reward thresholds in saline- and nicotine-treated rats. No differential effect of eticlopride on brain reward thresholds in saline- and nicotine-treated rats was observed. Decreased sensitivity to D1-like receptor antagonism in the posterior hypothalamus/anterior VTA may partly mediate the development of tolerance to the reinforcing effects of nicotine and the manifestation of negative affective signs associated with cessation of nicotine administration.

Animals↗
PubMed2005

Reward-based decision-making and aging.

Healthy aging is associated with a number of neuroanatomical and neurobiological alterations that result in various cognitive changes. Both, the dopaminergic as well as the serotonergic system are subject to change during aging. Receptor loss and severe structural changes in PFC and striatum have been reported. Aging is associated with a progressive decline in several cognitive functions, such as episodic memory, working memory, and processing speed. Furthermore, it is associated with deficits in tasks requiring adaptation to external feedback of right or wrong, or task-switching. Here, we develop the hypothesis that this loss of behavioral flexibility is caused by structural and functional alterations of the reward system leading to impairments in reward processing, learning stimulus reinforcement associations, and reward-based decision-making. We review (a) data on neural correlates and substrates of reward processing in young healthy animals and humans, (b) evidence for age related functional and structural alterations of the reward system, and (c) behavioral and neuroimaging data of age effects on reward-based decision-making processes. Implications for neuroeconomics and neurodegenerative diseases are discussed.

Aging↗
PubMed2006

Subjective sensitivity to monetary gradients is associated with frontolimbic activation to reward in cocaine abusers.

Drug addiction is characterized by marked disruptions in the ability to process reward. Here we evaluated in cocaine addicted and healthy control participants the subjective sensitivity to reward gradients and its association with neural responses to sustained reward. A self-report questionnaire was used to assess the former. A functional magnetic resonance imaging task that utilized monetary reward as feedback in a blocked design was used to assess the latter. Results revealed that whereas control subjects valued high money more than low money, over half of the cocaine addicted subjects valued all monetary amounts equally. This compromised subjective sensitivity to gradients in reward value was significantly correlated with higher activations to money in the lateral orbitofrontal cortex/inferior frontal gyrus (BA 47) and amygdala, and lower activations in the middle frontal gyrus (BA 6), which together explained 85% of the variability on this rating scale in the cocaine abusers only. These results provide for the first time evidence of restricted subjective sensitivity to gradients of reward in cocaine addiction and of the involvement of frontolimbic brain regions (including the orbitofrontal cortex) in this deficit.

Cocaine-Related Disorders↗
PubMed2006

The effect of graded monetary reward on cognitive event-related potentials and behavior in young healthy adults.

Temporal correlates of the brain circuit underlying reward processing in healthy adults remain unclear. The current study investigated the P3 and contingent negative variation (CNV) as putative reward-related temporal markers. The effect of sustained monetary reward on these event-related potentials and on behavior was assessed using a warned reaction-time paradigm in 16 young healthy subjects. Monetary reward (0, 1 and 45 cents) varied across blocks of trials. While the CNV was unaffected by money, P3 amplitude was significantly larger for 45 than the 1 and 0 cent conditions. This effect corresponded to the monotonically positive subjective ratings of interest and excitement on the task (45>1>0). These findings suggest a difference between the P3 and CNV; the P3 is sensitive to the sustained effect of relative reward value, while the CNV does not vary with reward magnitude.

Adult↗
PubMed2006

Sensitivity to reward and punishment and the prefrontal cortex in major depression.

BACKGROUND: Patients with major depressive disorder (MDD) show neuropsychological impairments, including deficient executive functions and altered sensitivity to reward and punishment. METHODS: Executive functions (Wisconsin Card Sorting Test, WCST) and contingency learning based on the cumulative effect of reward and punishment (Iowa Gambling Test, IGT) were assessed in 30 medicated patients with unipolar MDD and in 20 healthy control volunteers. In the classic ABCD version of the IGT, advantageous decks are characterized by immediate small reward but even smaller future punishment. In the modified EFGH version, advantageous decks are characterized by immediate large punishment but even larger future reward. RESULTS: Patients with MDD were impaired in the WCST and in the ABCD version of the IGT but showed normal performances on the EFGH task. Depression, but not executive dysfunctions, significantly predicted performances on the EFGH task: less severe depressive symptoms were associated with better performances on the EFGH task. LIMITATIONS: The sample size was small and only few neuropsychological tests were used. Unmedicated patients were not assessed. Individual personality style, response strategies, and behavioral impulsivity were not investigated. CONCLUSIONS: Medicated patients with MDD show altered sensitivity to reward and punishment: immediate large reward enhanced related response patterns even when the strategy was disadvantageous and immediate large punishment did not prohibit related response patterns. Impairments in emotional decision-making were not a pure consequence of executive dysfunctions.

Adult↗
PubMed2005

The effects of continuous and partial reward on the vigilance task performance of adults with attentional deficits: a pilot investigation.

The effects of reward schedule (100% and 30%) and extinction on attention (reaction time to auditory stimuli) and frustration levels (pressure exerted on a response key) of 15 adults with attentional disorders and 21 normal adults were examined using a continuous performance task. We predicted, that adults with attentional deficits would (a) perform similar to comparisons when rewarded on a continuous schedule, (b) exhibit higher levels of frustration when that continuous schedule was moved to an extinction schedule, and (c) experience more frustration than comparisons when rewarded on a partial schedule. Overall, adults with attentional deficits were slower to respond and their responses were more variable than typical comparisons across trials, similar to what is observed for children. Continuous reward resulted in poorer performance earlier in the reward phase and continued throughout an extinction phase. The frustration levels of adults with attentional deficits did not differ from comparisons across schedule conditions. Results are discussed in terms of the role of arousal in mediating responding to various schedules of reward.

Adult↗
PubMed2005

Activity in human reward-sensitive brain areas is strongly context dependent.

Functional neuroimaging research in humans has identified a number of brain areas that are activated by the delivery of primary and secondary reinforcers. The present study investigated how activity in these reward-sensitive regions is modulated by the context in which rewards and punishments are experienced. Fourteen healthy volunteers were scanned during the performance of a simple monetary gambling task that involved a "win" condition (in which the possible outcomes were a large monetary gain, a small gain, or no gain of money) and a "lose" condition (in which the possible outcomes were a large monetary loss, a small loss, or no loss of money). We observed reward-sensitive activity in a number of brain areas previously implicated in reward processing, including the striatum, prefrontal cortex, posterior cingulate, and inferior parietal lobule. Critically, activity in these reward-sensitive areas was highly sensitive to the range of possible outcomes from which an outcome was selected. In particular, these regions were activated to a comparable degree by the best outcomes in each condition-a large gain in the win condition and no loss of money in the lose condition-despite the large difference in the objective value of these outcomes. In addition, some reward-sensitive brain areas showed a binary instead of graded sensitivity to the magnitude of the outcomes from each distribution. These results provide important evidence regarding the way in which the brain scales the motivational value of events by the context in which these events occur.

Adult↗
PubMed2005

Dysfunction of ventral striatal reward prediction in schizophrenia.

BACKGROUND: Negative symptoms may be associated with dysfunction of the brain reward system in schizophrenia. We used functional magnetic resonance imaging (fMRI) to assess the BOLD response in the ventral striatum of unmedicated schizophrenics during presentation of reward-indicating and loss-indicating stimuli. METHODS: A total of 10 schizophrenic men (7 never medicated, 3 unmedicated for at least 2 years) and 10 age-matched healthy male volunteers participated in an incentive monetary delay task, in which visual cues predicted that a rapid response to a subsequent target stimulus would result either in monetary gain or loss or would have no consequence. RESULTS: Compared to healthy controls, unmedicated schizophrenics showed reduced ventral striatal activation during the presentation of reward-indicating cues. Decreased activation of the left ventral striatum was inversely correlated with the severity of negative (and trendwise positive) symptoms. DISCUSSION: Reduced activation in one of the central areas of the brain reward system, the ventral striatum, was correlated with the severity of negative symptoms in medication-free schizophrenics. In unmedicated schizophrenic patients, a high striatal dopamine turnover may increase the "noise" in the reward system, thus interfering with the neuronal processing of reward-predicting cues by phasic dopamine release. This, in turn, may contribute to negative symptoms as such as anhedonia, apathy, and loss of drive and motivation.

Adult↗
PubMed2006

Reward-motivated learning: mesolimbic activation precedes memory formation.

We examined anticipatory mechanisms of reward-motivated memory formation using event-related FMRI. In a monetary incentive encoding task, cues signaled high- or low-value reward for memorizing an upcoming scene. When tested 24 hr postscan, subjects were significantly more likely to remember scenes that followed cues for high-value rather than low-value reward. A monetary incentive delay task independently localized regions responsive to reward anticipation. In the encoding task, high-reward cues preceding remembered but not forgotten scenes activated the ventral tegmental area, nucleus accumbens, and hippocampus. Across subjects, greater activation in these regions predicted superior memory performance. Within subject, increased correlation between the hippocampus and ventral tegmental area was associated with enhanced long-term memory for the subsequent scene. These findings demonstrate that brain activation preceding stimulus encoding can predict declarative memory formation. The findings are consistent with the hypothesis that reward motivation promotes memory formation via dopamine release in the hippocampus prior to learning.

Adolescent↗
PubMed2005

Prolonged nicotine exposure does not alter GABA(B) receptor-mediated regulation of brain reward function.

Gamma-aminobutyric acid subtype B (GABA(B)) receptors play an important role in regulating brain reward function. Accumulating evidence suggests that chronic exposure to drugs of abuse may alter GABA(B) receptor function. The present studies investigated whether chronic nicotine administration, using a regimen that induces nicotine dependence, increased inhibitory regulation of brain reward function by GABA(B) receptors, as measured by intracranial self-stimulation (ICSS) thresholds in rats. Such an action of nicotine may contribute to the reward deficit observed during nicotine withdrawal. Nicotine-dependent and control rats received the GABA transaminase inhibitor gamma-vinyl-GABA or the GABA(B) receptor agonist CGP44532 according to a within-subjects Latin square design, and ICSS thresholds were assessed post-injection. Systemic administration of the lowest doses of GVG or CGP44532 did not alter reward thresholds in control or nicotine-treated rats, whereas the highest doses of each drug elevated thresholds similarly in both groups. Further, micro-infusion of CGP44532 directly into the ventral tegmental area elevated ICSS thresholds similarly in saline- and nicotine-treated rats. Overall, these data demonstrate that prolonged nicotine exposure did not alter GABA(B) receptor-mediated regulation of brain reward function, and suggest that alterations in GABA(B) receptor activity are unlikely to play a role in the brain reward deficits associated with spontaneous nicotine withdrawal.

4-Aminobutyrate Transaminase↗
PubMed2004

Is dopamine required for natural reward?

Reward is fundamental to the organization of behavior, and the neurotransmitter dopamine (DA) is widely recognized to be critical to the neurobiology of reward, learning and addiction. Virtually all drugs of abuse, including heroin and other opiates, alcohol, cocaine, amphetamine and nicotine activate dopaminergic systems. So called "natural" rewards such as food, positive social interactions and even humor, likewise activate DA neurons and are powerful aids to attention and learning. Sweet solutions are a well-characterized natural reward. When a source of sugar is encountered, animals will consume substantial amounts, return to it preferentially, and will work to obtain access. Dopamine systems are activated in animals drinking sugar solutions, and lesions of dopaminergic neurons or pharmacological blockade of DA receptors seem to reduce the reward value of both sweet tastes and drugs of abuse. However, we have recently demonstrated that genetically modified mice that cannot make DA (DD mice) manifest normal sucrose preference. During preference tests, mutant mice initiated licking less frequently than did normal mice, but the rate of licking by DD mice for sweets was actually higher than that of normal mice, indicating that their motor ability to lick is intact. We conclude that DA is not required for the hedonic response to sweets nor for their discrimination. This brief and slightly humorous review discusses these findings in the context of current and historical answers to the question, "What is the role of DA in reward?"

Animals↗
PubMed2006

Modulation of food reward by adiposity signals.

Extensive historical evidence from the drug abuse literature has provided support for the concept that there is functional communication between central nervous system (CNS) circuitries which subserve reward/motivation, and the regulation of energy homeostasis. This concept is substantiated by recent studies that map anatomical pathways, or which demonstrate that hormones and neurotransmitters associated with energy homeostasis regulation can directly modulate reward and motivation behaviors. Studies from our laboratory have focused specifically on the candidate adiposity hormones, insulin and leptin, and show that these hormones can decrease performance in behavioral paradigms that assess the rewarding or motivating properties of food. Additionally we and others have provided evidence that the ventral tegmental area may be one direct target for these effects, and we are currently exploring other potential anatomical targets. Finally, we are beginning to explore the interaction between adiposity signals, chronic maintenance diet of rats, and different types of food rewards to more closely simulate the current food environments of Westernized societies including the U.S. We propose that future studies of food reward should include a more complex environment in the experimental design that takes into account abundance and variety of rewarding foods, psychological stressors, and choices of reward modalities.

Adiposity↗
PubMed2004

Neuronal representations of cognitive state: reward or attention?

The effects of spatial or featural attention on the activity of neurons have been studied in many experiments that have used a variety of neurophysiological approaches. Other experiments have examined how expectations about reward are represented in neuronal activity in various brain regions. Although attention and reward are distinct concepts, I argue here that many neurophysiological experiments on attention and reward do not permit a clean dissociation between the two. This problem arises in part because reward contingencies are the only parameter manipulated in any of these experiments. I describe how attention and reward expectations have been confounded, giving rise to uncertainty about how signals related to attention and reward are distributed in the brain.

Animals↗