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PubMed2000

Effects of reward anticipation, reward presentation, and spatial parameters on the firing of single neurons recorded in the subiculum and nucleus accumbens of freely moving rats.

The subiculum is the major output of the hippocampal formation (involved in spatial processing). Subicular afferents innervate the nucleus accumbens, which is thought to integrate limbic reward information with motor output. Rats were chronically implanted with extra-cellular recording electrodes aimed at both structures to investigate the functional relationship between them. Animals were then trained on a spatial task in which they searched for random locations where they would receive rewarding medial forebrain bundle stimulation. At random times a cue tone was sounded, indicating that the reward location was in the center of the environment. Rats quickly learned to run to the center upon hearing the tone in order to receive a reward. Simultaneously recorded groups of up to eight subicular and accumbens neurons were found to display alterations in firing rate after rewarding medial forebrain bundle stimulation. Moreover, neurons in both subiculum and accumbens displayed alterations in firing rate prior to arrival at the center during cued runs, i.e. they anticipated predictable rewards. Subicular and accumbens firing was also correlated with spatial location. However, neurons in accumbens were more likely to respond to task events, and these responses were more varied, than those seen in subiculum. Thus, while convergence of spatial and reward information occurs at the level of single cells in both subiculum and nucleus accumbens, these structures also display functional localization.

Acoustic Stimulation↗
PubMed2000

Reward-predicting and reward-detecting neuronal activity in the primate supplementary eye field.

In addition to cells specifically active with visual stimuli, saccades, or fixation, the supplementary eye field contains cells that fire in precise temporal relationship with the occurrence of reward. We studied reward-related activity in two monkeys performing a prosaccade/antisaccade task and in one monkey trained in memory prosaccades only. Two types of neurons were distinguished by their reciprocal firing pattern: reward-predicting (RP) and reward-detecting (RD). RP neurons linearly increased their firing as early as 150 ms before saccade onset until the occurrence of reward, at which time they abruptly ceased firing. In contrast, RD neurons fired in phase with reward delivery, even when its duration was varied and when it was repeated at different frequencies. RD discharges were little affected or unaffected by the position of a visual cue that briefly anchored the goal at the onset of reward. The complementary firing patterns of the RP and RD neurons could provide a feedback mechanism necessary for learning and performing the task.

Animals↗
PubMed1989

Effects of reward and familiarity of reward agent on spontaneous play in preschoolers: a field study.

A field experiment was conducted with preschool children to test the effect of rewards on a familiar, spontaneous play activity, in conditions as close as possible to the children's natural school context, and to examine the role of familiarity of the person who administered rewards. In three experimental conditions, children were rewarded either by their own teacher or by an unknown adult for playing with toys at the school playground and stayed with either the teacher or the unknown adult in the remaining part of reward sessions. Spontaneous play was significantly reduced by the reward relative to baseline levels and recovered after a 3-wk. interval. However, no difference due to familiarity/unfamiliarity of reward agent could be found. Results, discussed in terms of an incentive contrast hypothesis, attest to the generality and external validity of the undermining effects of rewards.

Child, Preschool↗
PubMed1997

[Expectation of others' reward allocation, and ingroup favoritism in reward allocation].

The purpose of this study was to investigate people's expectation of others' ingroup favoritism, and the effect of expecting others to take part in reward allocation decision on ingroup favoritism in reward allocation. Subjects were randomly assigned to two groups, and were asked to rate attractiveness of ingroup members, and to allocate reward to ingroup and outgroup under two conditions. In the unilateral condition, the subject alone was to make the decision, and in the multilateral condition, every subject was to. The results indicated that equally in all conditions, subjects rated ingroup members more attractive, and expected others to allocate more reward to own groups. Reward allocation that favored ingroup occurred only under the multilateral condition, where everyone participated in reward allocation, regardless of whether the subject's own reward was dependent on others' decisions or was a fixed amount. The findings suggest that ingroup favoritism was not a result of quasi-strategy of self-interest in an attempt to maximize own gains, but of psychological group formation.

Adult↗
PubMed2025

Multi-Locus Pro-Dopaminergic Restoration of Reward Brain Circuitry in Reward Deficiency Rescinds Mono-Pharmaceutical Targeting.

Dopaminergic dysfunction in reward circuitry is well-documented as a contributor to addictive behaviors. Evidence indicates that changes in synchronous neural activity between brain regions mediating reward and cognitive functions may significantly contribute to substance-related disorders. In this commentary we highlight findings showing that the pro-dopaminergic nutraceutical (KB220) enhances functional connectivity between reward and cognitive brain areas in both animal and human studies. Animal studies demonstrate that KB220 activates important brain reward-related regions, including the nucleus accumbens, anterior cingulate gyrus, anterior thalamic nuclei, hippocampus, and prelimbic and infralimbic loci. Kb220 induced significant functional connectivity, enhanced neuroplasticity, and improved dopaminergic functionality within the brain reward circuitry with effects localized to these regions rather than broader distributed across the brain. In abstinent heroin-dependent individuals, acute KB220 administration significantly induced BOLD activation in caudate-accumbens dopaminergic pathways relative to placebo. Furthermore, data from 36 clinical trials and preclinical studies encompassing over 1,000 subjects, demonstrate that KB220 supports "dopamine homeostasis" across various reward deficiency behaviors. Clinical outcomes and quantitative electroencephalogy (qEEG) results underscore KB220's potential anti-craving/anti-relapse effects in addiction and other psychiatric disorders through direct or indirect dopaminergic modulation. Based on a review of the existing knowledge and further intensive investigation, we propose that instead of relying on mono-pharmaceutical approaches, the scientific community should endorse multi-loci dopaminergic restoration of reward brain circuitry as a fundamental paradigm for addressing mental illness.

Alcohol Use Disorder (AUD)↗
PubMed1983

Reward and aversive effects of lateral hypothalamic stimulation in rats measured by a modified runway and reward summation technique.

This report presents a refinement of the reward summation technique which has seen increasing use as a measure of the reward and performance factors associated with studies of the anatomical and neurochemical mechanisms of lateral hypothalamic stimulation. The technique involves determining the vigor of reward seeking behavior at a number of stimulation levels and making calculations upon this behavior/stimulation relationship. The refinement involves separating out the behavioral consequences of aversiveness which is often mixed with hypothalamic reward, particularly at high levels of stimulation. Specifically, it is shown that total running speed, the conventional measure of reward seeking behavior in a runway, is made of two components: running the runway and latency to press the reward lever. Furthermore, the latency-to-press the lever for any brain stimulation is positively correlated with latency to escape the same stimulation in an ON-OFF apparatus. Thus, latency-to-press likely is attributable to the aversiveness of the stimulation. Measuring only the first component is a more refined measure of the reward of brain stimulation.

Animals↗
PubMed1991

Measuring the subjective magnitude of brain stimulation reward by titration with rate of reward.

The magnitude of experienced reward as a function of the pulse frequency and current in trains of fixed duration delivered to the medial forebrain bundle of the rat was measured using a new psychophysical method in which the parameters of the brain stimulation reward on one lever are adjusted to offset the effect of changing the rate of reward on a competing lever. Subjective reward magnitude is a steep sigmoidal function of both pulse frequency and current. The growth of reward to its half-maximal level was approximated by a power function with an exponent that varied from 2 to 10. Within a subject, the exponent was the same for both current and pulse frequency, which supports the hypothesis that the magnitude of reward from a train of fixed duration is determined by the rate at which action potentials are generated in the population of reward-relevant axons (the counter hypothesis). This rate is proportional to Current x Pulse Frequency.

Animals↗
PubMed2006

The psychostimulant and rewarding effects of cocaine in histidine decarboxylase knockout mice do not support the hypothesis of an inhibitory function of histamine on reward.

RATIONALE AND OBJECTIVES: Lesion studies have shown that the tuberomammillary nucleus (TM) exerts inhibitory effects on the brain reward system. To determine whether histamine from the TM is involved in that reward inhibitory function, we assessed the stimulant and rewarding effects of cocaine in knockout mice lacking histidine decarboxylase (HDC KO mice), the histamine-synthesizing enzyme. If histamine actually plays an inhibitory role in reward, then it would be expected that mice lacking histamine would be more sensitive to the behavioral effects of cocaine. MATERIALS AND METHODS: The first experiment characterized spontaneous locomotion and cocaine-induced hyperactivity (0, 8, and 16 mg/kg, i.p.) in wild-type and HDC KO mice. The rewarding effects of cocaine were investigated in a second experiment with the place-conditioning technique. RESULTS: The first experiment demonstrated that histidine decarboxylase mice showed reduced exploratory behaviors but normal habituation to the test chambers. After habituation to the test chambers, HDC KO mice were slightly, but significantly, less stimulated by cocaine than control mice. This finding was replicated in the second experiment, when cocaine-induced activity was monitored with the place-conditioning apparatus. Furthermore, a significant place preference was present in both genotypes for 8 and 16 mg/kg cocaine, but not for 2 and 4 mg/kg. CONCLUSIONS: Our data confirm previous results demonstrating that HDC KO mice show reduced exploratory behaviors. However, contrary to the hypothesis that histamine plays an inhibitory role in reward, histamine-deficient mice were not more responsive to the psychostimulant effects of cocaine.

Animals↗
PubMed1993

Amygdala modulates memory for changes in reward magnitude: reversible post-training inactivation with lidocaine attenuates the response to a reduction in reward.

The present study used a reward reduction paradigm to examine the role of the amygdala in memory for reduction in reward magnitude. Male Sprague-Dawley rats were implanted with bilateral amygdala cannulae and trained to run a straight alley (6 trials/day) for either ten or one 45-mg food pellets. On Day 10 of training, half the animals in the 10 pellet reward group were shifted to a one pellet reward. Immediately following shifted trials, the animals received an intra-amygdala injection of either a 2% lidocaine solution or phosphate buffer (0.5 microliter/side). Shifted training continued for 2 more days and no further injections were given. Shifted animals that received a buffer injection displayed a sharp increase in response latencies compared to unshifted controls on the second day of shifted training. In contrast, shifted animals that received intra-amygdala injections of lidocaine exhibited significantly lower latencies compared to the shifted vehicle group on the second day of shifted training. The findings indicate that post-training inactivation of the amygdala attenuates the response to reward reduction, suggesting that the amygdala modulates the storage for a reduction in reward magnitude.

Amygdala↗
PubMed2000

Extending overjustification: the effect of perceived reward-giver intention on response to rewards.

The perceived intention model incorporates a new moderator, beliefs about reward-giver intention, into the overjustification paradigm. In 2 simulated shopping studies featuring products paired with promotional rewards, consumers who believed the marketer was promotion focused (reward used to encourage purchase) reported lower purchase intentions and brand attitudes for promoted products after promotion, whereas consumers who believed the marketer was reward focused (promotion used to distribute the reward) showed no attitude change. Promotion-focus beliefs lowered attitudes by heightening the contingency between the promotion and purchase and thereby increasing the perceived causal role of the reward. This effect was contingent on initial behavior--postpromotion attitude change occurred for consumers who actively engaged in product decisions but not for consumers who passively observed the choice sets.

Adult↗
PubMed2005

Active immunisation against nicotine blocks the reward facilitating effects of nicotine and partially prevents nicotine withdrawal in the rat as measured by dopamine output in the nucleus accumbens, brain reward thresholds and somatic signs.

We recently showed that active immunisation with the nicotine immunoconjugate IP18-KLH reduces the nicotine-induced increase in dopamine (DA) output in the nucleus accumbens (NAC) and prevents reinstatement of nicotine-seeking behaviour in rats. These effects are mediated by altered distribution of nicotine, resulting in reduced amounts of nicotine reaching the brain, thereby interfering with the rewarding properties of the drug. The present study was designed to explore the effect of immunisation against nicotine on mecamylamine-precipitated nicotine withdrawal as assessed by the reduction in DA output in the NAC in rats. Measuring brain reward thresholds and somatic signs of nicotine withdrawal, the effects of immunisation were also tested during chronic nicotine treatment and after its withdrawal. Finally, we examined the effect of immunisation on challenge injections of nicotine on brain reward thresholds after the increases in somatic signs and reward thresholds associated with nicotine withdrawal had dissipated. The results show that immunisation with IP18-KLH prevented the decrease in DA output in the NAC associated with mecamylamine-precipitated nicotine withdrawal. Moreover, immunisation against nicotine did not precipitate a withdrawal syndrome, as measured by brain reward thresholds and somatic signs, in rats chronically exposed to nicotine. Furthermore, the withdrawal syndrome elicited after cessation of chronic nicotine administration was attenuated in immunised rats compared to that of mock-immunised rats. Finally, the lowering in reward thresholds after nicotine challenge injections was attenuated in both naïve and previously nicotine-exposed immunised rats. In conclusion, the present results show that immunisation with IP18-KLH did not precipitate nicotine withdrawal in rats. Thus, immunisation with IP18-KLH may not elicit nicotine withdrawal in smokers either. Furthermore, since the withdrawal syndrome in rats was attenuated by immunisation, the nicotine withdrawal in smokers should not be worsened but may even be ameliorated during a quit attempt.

Animals↗
PubMed2005

Delay discounting of real and hypothetical rewards III: steady-state assessments, forced-choice trials, and all real rewards.

Human research in delay discounting has omitted several procedures typical of animal studies: forced-choice trials, consequences following each response, and assessment of stable response patterns. The present study manipulated these procedures across two conditions in which real or hypothetical rewards were arranged. Six college students participated in daily sessions, in which steady-state discounting of hypothetical and real rewards was assessed. No systematic effects of repeated exposure to hypothetical rewards was detected when compared with first day assessments of discounting. Likewise, no systematic effect of reward type (real versus hypothetical) was detected. When combined with previous research failing to detect a difference between hypothetical and potentially real rewards, these findings suggest that assessing discounting of hypothetical rewards in single sessions is a practical and valid procedure in the study of delay discounting.

Adaptation, Psychological↗
PubMed1990

Role of reward and enhancement of conditioned reward in persistence of responding for cocaine.

The primary rewarding effects of cocaine, based presumably on its powerful euphoric properties, are widely recognized and have been implicated as a major factor in the abuse potential of this drug. Several different experimental procedures have been developed to study the rewarding properties of cocaine in animals, and three of the most influential techniques, namely intravenous self-administration, pharmacological enhancement of brain-stimulation reward, and conditioned place preference, are described briefly. A related influence of cocaine that may also contribute to its strong control over behavior is the enhancement of the effects of conditioned rewarding stimuli. Experiments that exemplify this phenomenon are described along with those that relate to its neural substrates. Accordingly, the argument is advanced that the compulsion to abuse cocaine may be based on two distinct effects; (1) primary reward related to euphoria and (2) a more subtle but equally potent influence by which the drug amplifies or enhances the effects of conditioned rewarding stimuli. The final section of the paper reviews the literature pertaining to the facilitation of extinction by neuroleptic drugs. A combined behavioral pharmacologic intervention, involving extinction procedures in conjunction with neuroleptic treatment, is proposed as a potential therapeutic strategy for breaking the cocaine habit in humans.

Journal Article↗
PubMed2004

Reward representations and reward-related learning in the human brain: insights from neuroimaging.

This review outlines recent findings from human neuroimaging concerning the role of a highly interconnected network of brain areas including orbital and medial prefrontal cortex, amygdala, striatum and dopaminergic mid-brain in reward processing. Distinct reward-related functions can be attributed to different components of this network. Orbitofrontal cortex is involved in coding stimulus reward value and in concert with the amygdala and ventral striatum is implicated in representing predicted future reward. Such representations can be used to guide action selection for reward, a process that depends, at least in part, on orbital and medial prefrontal cortex as well as dorsal striatum.

Animals↗
PubMed2004

Bilateral orbital prefrontal cortex lesions in rhesus monkeys disrupt choices guided by both reward value and reward contingency.

The orbital prefrontal cortex (PFo) operates as part of a network involved in reward-based learning and goal-directed behavior. To test whether the PFo is necessary for guiding behavior based on the value of expected reward outcomes, we compared four rhesus monkeys with two-stage bilateral PFo removals and six unoperated controls for their responses to reinforcer devaluation, a task that assesses the monkeys' abilities to alter choices of objects when the value of the underlying food has changed. For comparison, the same monkeys were tested on a standard test of flexible stimulus-reward learning, namely object reversal learning. Relative to controls, monkeys with bilateral PFo removals showed a significant attenuation of reinforcer devaluation effects on each of two separate assessments, one performed shortly after surgery and the other approximately 19 months after surgery; the operated monkeys were also impaired on object reversal learning. The same monkeys, however, were unimpaired in acquisition of object discrimination learning problems and responded like controls when allowed to choose foods alone, either on a food preference test among six different foods or after selective satiation. Thus, satiety mechanisms and the ability to assign value to familiar foods appear to be intact in monkeys with PFo lesions. The pattern of results suggests that the PFo is critical for response selection based on predicted reward outcomes, regardless of whether the value of the outcome is predicted by affective signals (reinforcer devaluation) or by visual signals conveying reward contingency (object reversal learning).

Animals↗
PubMed2005

[Natural rewarding and drug rewarding].

In the brain of animals and humans there is a rewarding mechanism to encourage the behavior that is beneficial for the living of the individual and for the prolongation of the generation. However, when this system is being abused by drugs of addiction, chronic adaptive changes may occur that would cause serious damage to the organism. The neural substrate of the rewarding system is mainly based on the dopaminergic pathway, starting from the ventral tegmental area of the midbrain and ended in the nucleus accumbens of the limbic brain. This pathway serves both natural rewarding such as food and sex as well as drug rewarding such as heroin and cocaine. This paper is aimed to discuss the similarities and differences between the natural and drug-induced rewarding in an attempt to block the latter without affecting the former.

Animals↗
PubMed2000

Intra-accumbens amphetamine increases the conditioned incentive salience of sucrose reward: enhancement of reward "wanting" without enhanced "liking" or response reinforcement.

Amphetamine microinjection into the nucleus accumbens shell enhanced the ability of a Pavlovian reward cue to trigger increased instrumental performance for sucrose reward in a pure conditioned incentive paradigm. Rats were first trained to press one of two levers to obtain sucrose pellets. They were separately conditioned to associate a Pavlovian cue (30 sec light) with free sucrose pellets. On test days, the rats received bilateral microinjection of intra-accumbens vehicle or amphetamine (0.0, 2.0, 10.0, or 20.0 microgram/0.5 microliter), and lever pressing was tested in the absence of any reinforcement contingency, while the Pavlovian cue alone was freely presented at intervals throughout the session. Amphetamine microinjection selectively potentiated the cue-elicited increase in sucrose-associated lever pressing, although instrumental responding was not reinforced by either sucrose or the cue during the test. Intra-accumbens amphetamine can therefore potentiate cue-triggered incentive motivation for reward in the absence of primary or secondary reinforcement. Using the taste reactivity measure of hedonic impact, it was shown that intra-accumbens amphetamine failed to increase positive hedonic reaction patterns elicited by sucrose (i.e., sucrose "liking") at doses that effectively increase sucrose "wanting." We conclude that nucleus accumbens dopamine specifically mediates the ability of reward cues to trigger "wanting" (incentive salience) for their associated rewards, independent of both hedonic impact and response reinforcement.

Amphetamine↗
PubMed1991

Olfactory associative conditioning in infant rats with brain stimulation as reward: II. Norepinephrine mediates a specific component of the bulb response to reward.

One of the circuits modified by early olfactory learning is in the olfactory bulb. Specifically, response patterns of mitral-tufted cells are modified by associative conditioning during the early postnatal period. In addition, previous work has demonstrated that mitral-tufted cell single units respond to both olfactory conditioned stimuli and rewarding stimulation of the medial forebrain bundle-lateral hypothalamus (MFB-LH). The present study suggests that norepinephrine beta-receptor activation is required for early olfactory learning using MFB-LH stimulation as reward. Propranolol injected before odor-MFB-LH pairings blocks the acquisition of conditioned behavioral responses and their neural correlates to the conditioned odor. Furthermore, propranolol blocks a specific class of the mitral-tufted cell responses to MFB-LH reward stimulation. The relationship of this response to reward and early learning is discussed.

Aging↗