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At least 235 records · Page 13Linked to original sources
PubMed2004

Differential encoding of information about progress through multi-trial reward schedules by three groups of ventral striatal neurons.

In the course of daily activity we continually judge whether the goal sought is worth the work that must be done to obtain it. The ventral striatum is thought to play a central role in making such judgments. When reward schedules are used to investigate these judgments ventral striatum neurons show responses near the time of the cue, the bar-release, and/or the reward delivery. We evaluated the type of coding that occurs at these three time points by using codes or factorizations with: (1) two states for reward versus non-reward, (2) four states for the progress in the reward schedule, and (3) six states for all of the states of the schedule, quantified using information theory and ANOVA. For the bar-release- and reward-related responses the percent variance explained was as high for the two states code as with the six states code. The information for the four state code rose slightly but significantly for the bar-release-related neurons. For the cue-related neurons the code with six states carried more information than the simpler codes. Thus, responses at different times appear to play different roles. Responses occurring early in trials differentiate all states, i.e., the path to a reward, whereas those late in trials code knowledge of impending reward.

Action Potentials↗
PubMed2004

An fMRI study of reward-related probability learning.

The human striatum has been implicated in processing reward-related information. More recently, activity in the striatum, particularly the caudate nucleus, has been observed when a contingency between behavior and reward exists, suggesting a role for the caudate in reinforcement-based learning. Using a gambling paradigm, in which affective feedback (reward and punishment) followed simple, random guesses on a trial by trial basis, we sought to investigate the role of the caudate nucleus as reward-related learning progressed. Participants were instructed to make a guess regarding the value of a presented card (if the value of the card was higher or lower than 5). They were told that five different cues would be presented prior to making a guess, and that each cue indicated the probability that the card would be high or low. The goal was to learn the contingencies and maximize the reward attained. Accuracy, as measured by participant's choices, improved throughout the experiment for cues that strongly predicted reward, while no change was observed for unpredictable cues. Event-related fMRI revealed that activity in the caudate nucleus was more robust during the early phases of learning, irrespective of contingencies, suggesting involvement of this region during the initial stages of trial and error learning. Further, the reward feedback signal in the caudate nucleus for well-learned cues decreased as learning progressed, suggesting an evolving adaptation of reward feedback expectancy as a behavior-outcome contingency becomes more predictable.

Adult↗
PubMed2006

Sensitivity of the nucleus accumbens to violations in expectation of reward.

This study examined whether ventral frontostriatal regions differentially code expected and unexpected reward outcomes. We parametrically manipulated the probability of reward and examined the neural response to reward and nonreward for each probability condition in the ventral striatum and the orbitofrontal cortex (OFC). By late trials of the experiment, subjects showed slower behavioral responses for the condition with the lowest probability of reward, relative to the condition with the highest probability of reward. At the neural level, both the nucleus accumbens (NAcc) and OFC showed greater activation to rewarded relative to nonrewarded trials, but the accumbens appeared to be most sensitive to violations in expected reward outcomes. These data suggest distinct roles for frontostriatal circuitry in reward prediction and in responding to violations in expectations.

Adult↗
PubMed2006

Neural correlates of reward and attention in macaque area LIP.

Saccade reaction times decrease and the frequency of target choices increases with the size of rewards delivered for orienting to a particular visual target. Similarly, increasing rewards for orienting to a visual target enhances neuronal responses in the macaque lateral intraparietal area (LIP), as well as other brain areas. These observations raise several questions. First, are reward-related modulations in neuronal activity in LIP, as well as other areas, spatially specific or more global in nature? Second, to what extent does reward modulation of neuronal activity in area LIP reflect changes in visual rather than motor processing? And third, to what degree are reward-related modulations in LIP activity independent of performance-related modulations thought to reflect changes in attention? Here we show that increasing the size of fluid rewards in blocks reduced saccade reaction times and improved performance in monkeys performing a peripherally-cued saccade task. LIP neurons responded to visual cues spatially segregated from the saccade target, and for many neurons visual responses were systematically modulated by expected reward size. Neuronal responses also were positively correlated with reaction times independent of reward size, consistent with re-orienting of attention to the saccade target. These observations suggest that motivation and attention independently contribute to the strength of sustained visual responses in LIP. Our data thus implicate LIP in the integration of the sensory, motor, and motivational variables that guide orienting.

Action Potentials↗
PubMed2005

The effects of non-contingent extrinsic and intrinsic rewards on memory consolidation.

Emotional and arousing treatments given shortly after learning enhance delayed memory retrieval in animal and human studies. Positive affect and reward induced prior to a variety of cognitive tasks enhance performance, but their ability to affect memory consolidation has not been investigated before. Therefore, we investigated the effects of a small, non-contingent, intrinsic or extrinsic reward on delayed memory retrieval. Participants (n=108) studied and recalled a list of 30 affectively neutral, imageable nouns. Experimental groups were then given either an intrinsic reward (e.g., praise) or an extrinsic reward (e.g., US 1 dollar). After a one-week delay, participants' retrieval performance for the word list was significantly better in the extrinsic reward groups, whether the reward was expected or not, than in controls. Those who received the intrinsic reward performed somewhat better than controls, but the difference was not significant. Thus, at least some forms of arousal and reward, even when semantically unrelated to the learned material, can effectively modulate memory consolidation. These types of treatments might be useful for the development of new memory intervention strategies.

Adolescent↗
PubMed2004

Brain reward deficits accompany naloxone-precipitated withdrawal from acute opioid dependence.

Single injections with morphine can induce a state of acute opioid dependence in humans and animals, typically measured as precipitated withdrawal when an antagonist such as naloxone is administered 4-24 h after morphine. Repeated treatment with morphine results in a progressive shift in potency of naloxone to produce such acute withdrawal signs. The current study examined alterations in brain reward thresholds after acute and repeated treatment with morphine (5.6 mg/kg) using a discrete-trial current-intensity brain-stimulation reward procedure. Rats with stimulation electrodes aimed at the medial forebrain bundle at the level of the lateral hypothalamus were tested in twice daily sessions separated by 4 h. Separate groups of rats received treatment with morphine immediately after the first daily test session, and one of several doses of naloxone (0.10, 0.33, 1.0 mg/kg) 4 h later and immediately before the second session; these morphine and naloxone treatments were repeated for four consecutive days (Morphine-Repeat NAL). Additional groups examined the independent contribution of repeated morphine or repeated naloxone. One control group (Morphine-Vehicle) received morphine on all four treatment days, but vehicle before the second test session. A second group (Morphine-Single NAL) also received morphine on all four treatment days, but received 1.0 mg/kg only once after the final morphine pretreatment. A final control group received no morphine at all but received the 1.0-mg/kg dose of naloxone four times (Vehicle-Repeat NAL) before the second daily test session. Repeated naloxone alone (Vehicle-Repeat NAL) produced no changes in brain reward thresholds. Repeated morphine alone (Morphine-Vehicle) failed to alter reward thresholds measured 4 h postmorphine, but produced a slight increase in thresholds in the test sessions that occurred before morphine treatment on Days 3 and 4 (and hence 23.5 h after the previous day's morphine injection). This suggested the development of a modest spontaneous withdrawal-induced reward deficit measurable at 23.5 but not 4 h postmorphine. Naloxone dose-dependently increased brain reward thresholds 4 h after a single morphine pretreatment, with a further shift to the left in the naloxone dose-effect function resulting from repeated morphine and naloxone administration (Morphine-Repeat NAL). However, when the highest dose of naloxone was tested only after the final morphine pretreatment (Morphine-Single NAL), its potency was no different than when administered after the first morphine pretreatment. The results indicate that neuroadaptation within brain reward circuitry results in significant reward deficits after a single morphine pretreatment, and this deficit increases rapidly with repeated morphine and naloxone-induced withdrawal experience.

Acute Disease↗
PubMed1994

Comparison of delta opiate receptor agonist induced reward and motor effects between the ventral pallidum and dorsal striatum.

The role of the ventral pallidum and the dorsal striatum in mediating the rewarding effects of the delta receptor specific agonist [2-D-penicillamine, 5-D-penicillamine]enkephalin (DPDPE) were evaluated in the rat using the intracranial self-stimulation paradigm. Reward shifts were indicated by the change in frequency required to maintain half-maximal responding while motor/performance changes were identified by increases or decreases in the maximum responding. Each hour-long test session consisted of three identical, consecutive 20 min rate-frequency curves. In an effort to ascertain possible heterogeneity of function along the rostrocaudal axis, DPDPE (0.0 nmol = saline dose, 0.3 nmol = low dose, 1.0 nmol = medium dose, 3.0 nmol = high dose) was microinjected into either the rostral or caudal region of the two structures. Microinjections into the caudate were positioned directly above the ventral pallidum placements resulting in centromedial or caudomedial caudate placements. DPDPE microinjections into the rostral ventral pallidum resulted in a significant reward increase (28% increase or -0.14 log Hg shift) only at the high dose. In contrast, caudal ventral pallidal DPDPE microinjections showed a dose-response effect with reward increases of 19, 22 and 31% (-0.09, -0.11 and -0.16 log Hz) for the low, medium and high dose, respectively. DPDPE microinjections into the centromedial caudate resulted in a large reward increase (29% or -0.15 log Hz) at the high dose, while caudomedial caudate DPDPE microinjections had no effect on reward. Motor/performance effects tended to follow the pattern of reward effects, with most regions showing motor increases ranging from 25 to 75% over baseline activity. The only exception was found in the caudomedial caudate, where microinjections of the high dose of DPDPE resulted in an approximate 20% suppression of motor/performance activity. These results demonstrate that the ventral pallidum and the mediocentral caudate play a role in modulating opiate rewards, and adds to the growing body of literature regarding the regional heterogeneity within the caudate and ventral pallidum.

Animals↗
PubMed2002

Does neuropeptide Y contribute to the modulation of brain stimulation reward by chronic food restriction?

The rewarding effect produced by electrically stimulating particular sites in the lateral hypothalamus (LH) can be enhanced by chronic food restriction and body weight loss. The impact on brain stimulation reward (BSR) of certain hormones involved in the regulation of energy balance, such as leptin and corticotropin-releasing hormone, depends upon the sensitivity of BSR to food restriction. The present investigation assessed the influence of neuropeptide Y (NPY), a potent orexigenic peptide, on BSR generated by stimulating restriction-sensitive and -insensitive sites in the LH. Twelve male Long Evans rats were trained to press a lever for a rewarding train of stimulation. Rate-frequency curves, reflecting the number of rewards earned as a function of the stimulation frequency, were collected during free-feeding and then again following a period of food restriction and 20-25% body weight loss. NPY (4 microg) was administered intraventriculary during the food restriction condition. Alterations in the rewarding effect of the stimulation were assessed by measuring changes in the frequency required to maintain half-maximal rewards earned (M-50). In half of the subjects, food restriction produced significant decreases in M-50 values, indicating that the reward effectiveness of the stimulation was potentiated. In contrast, M-50 values were unaltered by food restriction in the remaining six animals. In most of the subjects in which M-50 values decreased following chronic food restriction, NPY failed to alter BSR. Similarly, BSR was unchanged by NPY administration in most of the rats with restriction-insensitive stimulation sites. These findings suggest that NPY does not take part in the process whereby food restriction and leptin modulate reward circuitry activated by stimulating restriction-sensitive sites.

Analysis of Variance↗
PubMed1997

Monkeys can associate visual stimuli with reward delayed by 1 s even after perirhinal cortex ablation, uncinate fascicle section or amygdalectomy.

In the present experiment monkeys learned concurrent associations of two-dimensional objects (presented on a computer screen) with delayed reward. Hypothetical mechanisms of associative memory, such as long-term potentiation (LTP), required coincidental activation of two population of neurons: one representing the object and the other signalling the reward. In monkeys neurons in area TE of temporal cortex show object-specific activity during object presentation but only fraction of those neurons remain active after stimulus offset. In a delayed reward condition the majority of object-specific neurons in TE cease firing before reward is given and can be detected. In the present study the rate of learning with 1000 ms delay of reward was no slower than learning with immediate reward. This indicates that information about the object is somehow retained across the delay, possibly somewhere outside TE. In the present study we tested that assumption. Area TE projects to the perirhinal cortex and, via uncinate fascicle, to the prefrontal cortex. In our hands, ablations of perirhinal cortex or disconnection of prefrontal cortex from TE (by transection of uncinate fascicle) did not impair learning with delayed reward. Ablation of amygdala, a structure involved in reward-learning, slowed down learning equally with and without delay. We conclude that retaining information about the visually perceived objects across a delay does not exclusively depend upon integrity of perirhinal cortex, or uncinate fascicle, or amygdala. Parallel involvement of those structures remains a possibility and establishment of the role of residual activity of TE neurons requires further neurophysiological investigation.

Amygdala↗
PubMed2001

Drug addiction, dysregulation of reward, and allostasis.

This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drug-taking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and relapse.

Animals↗
PubMed2000

Dissociation of primary and secondary reward-relevant limbic nuclei in an animal model of relapse.

The neural substrates underlying relapse to drug-seeking behavior after chronic drug abuse may differ from those underlying immediate drug-taking behavior. In a model of relapse to drug-seeking behavior following chronic cocaine self-administration and prolonged extinction, we have previously shown that rats will significantly reinstate lever responding for either primary reward (cocaine) or secondary reward (tone + light stimulus previously paired with cocaine). In the present study, we utilized reversible inactivation of discrete brain nuclei with tetrodotoxin (TTX) in order to examine the neural substrates mediating primary and secondary cocaine reward in rats allowed two weeks of cocaine self-administration. After one week of daily extinction sessions, bilateral inactivation of the basolateral amygdala resulted in significant attenuation of lever pressing for a cocaine-conditioned reward (tone + light). Following three more days of extinction, bilateral TTX inactivation of the basolateral amygdala had no effect on the reinstatement of cocaine self-administration. In contrast, TTX inactivation of the nucleus accumbens produced the exact opposite effects, with significant blockade of primary reward (cocaine alone), but not secondary reward (tone + light). Thus, cocaine-conditioned reward is neuroanatomically dissociated from primary cocaine reward.

Amygdala↗
PubMed2002

Getting formal with dopamine and reward.

Recent neurophysiological studies reveal that neurons in certain brain structures carry specific signals about past and future rewards. Dopamine neurons display a short-latency, phasic reward signal indicating the difference between actual and predicted rewards. The signal is useful for enhancing neuronal processing and learning behavioral reactions. It is distinctly different from dopamine's tonic enabling of numerous behavioral processes. Neurons in the striatum, frontal cortex, and amygdala also process reward information but provide more differentiated information for identifying and anticipating rewards and organizing goal-directed behavior. The different reward signals have complementary functions, and the optimal use of rewards in voluntary behavior would benefit from interactions between the signals. Addictive psychostimulant drugs may exert their action by amplifying the dopamine reward signal.

Animals↗
PubMed1999

Early developments in the ability to understand the relation between stimulus and reward.

Delayed nonmatching to sample (DNMS) is used to test the recognition memory function dependent on the medial temporal lobe. Children cannot succeed on this task until about 21 months. Because robust recognition is present well before then, the late emergence of another ability must account for the late success on DNMS. Evidence is presented here that the critical late-maturing competence is the ability to grasp the relation between stimulus and reward--that is, to understand that the stimulus is a symbol or marker for the reward. Infants of 9 and 12 months were tested on 3 conditions of DNMS. A sample object was presented. After a delay, the sample and a novel object appeared; choice of the novel object was rewarded. In the standard task, the reward was in a well beneath the stimulus. In the verbal-reward condition the reward was not a separate object but was praise and applause. In the Velcro condition, the reward, although a separate and separable object, was attached to the base of the stimulus. Most infants at both ages succeeded in the verbal-reward and Velcro conditions but not in the standard condition.

Adult↗
PubMed1999

Amount of reward has opposite effects on the discounting of delayed and probabilistic outcomes.

Previous research has shown that the value of large future rewards is discounted less steeply than is the value of small future rewards. These experiments extended this line of research to probabilistic rewards. Two experiments replicated the standard findings for delayed rewards but demonstrated that amount has an opposite effect on the discounting of probabilistic rewards. That is, large probabilistic amounts were discounted at the same or higher rates than small amounts. Although amount had opposite effects on the discounting of delayed and probabilistic rewards, nevertheless, the same form of mathematical function accurately described discounting of both types of reward. The findings suggest that fundamentally similar, but not identical, processes are involved in decision making regarding delayed and probabilistic rewards. The implications of these findings for impulsivity and self-control are discussed.

Adolescent↗
PubMed1998

Characteristics of basolateral amygdala neuronal firing on a spatial memory task involving differential reward.

Previous research has shown that spatial, movement, and reward information is integrated within the ventral striatum (VS). The present study examined the possible contribution of the basolateral nuclei of the amygdala (BLA) to this interaction by examining behavioral correlates of BLA neurons while rats performed multiple memory trials on an 8-arm radial maze. Alternate arms consistently held 1 of 2 different amounts of reward. Recorded cells were correlated with motion, auditory input, space, and reward acquisition. Reward-related units were found that anticipated reward encounter, that responded during reward consumption, and that differentiated between high and low reward magnitude. This is consistent with the hypothesis that BLA neurons may provide the VS with reward-related information that could then be integrated with spatial information to ultimately affect goal-directed behavior.

Amygdala↗
PubMed2001

GABA(A) receptors in the ventral tegmental area control bidirectional reward signalling between dopaminergic and non-dopaminergic neural motivational systems.

In the midbrain ventral tegmental area (VTA), both dopaminergic and nondopaminergic neural substrates mediate various behavioural reward phenomena. VTA GABAergic neurons are anatomically positioned to influence the activity of both the mesolimbic dopamine system and nondopamine efferents from the VTA. In order to examine the possible functional role of VTA GABA(A) receptors in neural reward processes, we performed discrete, bilateral microinjections of the GABA(A) receptor agonist, muscimol, or the GABA(A) receptor antagonist, bicuculline, into the VTA. Using a fully counterbalanced, unbiased conditioned place-preference paradigm, we demonstrate that activation of VTA GABA(A) receptors, with the GABA(A) receptor agonist muscimol (5--50 ng/microL), or inhibition of VTA GABA(A) receptors, with the GABA(A) receptor antagonist bicuculline (5--50 ng/microL), both produce robust rewarding effects. Furthermore, these rewarding effects can be pharmacologically dissociated: blockade of dopamine receptors with a dopamine receptor antagonist, alpha-flupenthixol (0.8 mg/kg; i.p.), or concurrent activation of VTA GABA(B) receptors with a GABA(B) receptor agonist, baclofen (70 ng/microL), blocked the rewarding properties of the GABA(A) receptor agonist, but had no effect on the rewarding properties of the GABA(A) receptor antagonist. These results suggest that, within the VTA, a single GABA(A) receptor substrate controls bidirectional reward signalling between dopaminergic and nondopaminergic brain reward systems.

Animals↗
PubMed2003

Low dose cocaine self-administration transiently increases but high dose cocaine persistently decreases brain reward function in rats.

This study investigated the effects of self-administered cocaine on brain reward function, measured by intracranial self-stimulation (ICSS) reward thresholds in rats. Self-administration of 10 and 20 cocaine injections (0.25 mg per injection, equivalent to 4.94 +/- 0.23 and 9.88 +/- 0.46 mg/kg, self-administered over 40 +/- 6.9 and 99 +/- 11.9 min, respectively) lowered reward thresholds 15 min later, indicating a facilitation of rewarding ICSS, but had no effect at 2, 24 or 48 h after administration. Thus, self-administration of low cocaine doses did not cause persistent changes in brain reward function. Forty cocaine injections (19.64 +/- 0.94 mg/kg; self-administered over 185 +/- 10.9 min) also transiently lowered reward thresholds 15 min later, while significant threshold current elevations were observed at 2 and 24 h after administration, indicating persistent withdrawal-like reward deficits. Finally, 80 cocaine injections (39.53 +/- 1.84 mg/kg, self-administered over 376 +/- 19.9 min) significantly elevated thresholds 2 and 48 h after self-administration, but not at 24 h. Threshold currents also tended to be elevated 15 min after self-administration. Overall, these data suggest that as the amount of self-administered cocaine increases the motivation to consume further cocaine may be shifted, from obtaining the rewarding actions of cocaine to avoidance and alleviation of a cocaine-induced negative affective state.

Animals↗
PubMed2000

Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors.

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome.

Behavior, Addictive↗