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PubMed2001

Neurons in rat medial prefrontal cortex show anticipatory rate changes to predictable differential rewards in a spatial memory task.

The present study electrophysiologically examined the contribution of prelimbic and infralimbic neurons in the medial prefrontal cortex (mPFC) to integration of reward and spatial information while rats performed multiple memory trials on a differentially rewarded eight arm radial maze. Alternate arms consistently held one of two different reward amounts. Similar to previous examinations of the rat mPFC, few cells showed discrete place fields or altered firing during a delay period. The most common behavioral correlate was a change in neuronal firing rate prior to reward acquisition at arm ends. A small number of reward-related cells differentiated between high and low reward arms. The presence of neurons that anticipate expected reward consequences based on information about the spatial environment is consistent with the hypothesis that the mPFC is part of a neural system which merges spatial information with its motivational significance.

Amygdala↗

PubMed1994

Midazolam administered to rats induces anterograde amnesia for changes in reward magnitude.

L. P. Crespi (1942) showed that rats trained to run an alley for a large food reward slowed down when shifted to a small reward. This effect is usually interpreted as an aversive emotional response to reward reduction (A. Amsel, 1958). Benzodiazepines attenuate the behavioral effects of reward reduction (cf. C. F. Flaherty, 1990), but the emphasis has been on their anxiolytic, not memory-impairing, effects. Researchers trained rats (175-200 g) to run an alley for food until asymptote was reached. Reward magnitude was then either decreased (Experiment 1) or increased (Experiment 2). The benzodiazepine midazolam (1 mg/kg ip), injected immediately prior to a decrease or increase in reward magnitude, impaired the later retention of both changes in a manner consistent with anterograde amnesia. The findings suggest that the memory-impairing effects of benzodiazepines may, at least in part, influence the response to reward reduction.

Animals↗

PubMed2005

Espresso reward learning, hold the dopamine: theoretical comment on Robinson et al. (2005).

QUESTION: Is dopamine needed for reward learning? ANSWER: No--at least, not in the brain of a caffeinated dopamine-deficient (DD) mutant mouse. That is the conclusion of an important paper in this issue by S. Robinson, S. M. Sandstrom, V. H. Denenberg, and R. D. Palmiter (see record 2005-01705-001). Those authors demonstrate that reward learning can proceed normally in the brains of DD mice, even though they contain no dopamine at the time of learning, if the mice are given caffeine just before learning. Caffeine activates the DD mice by a nondopaminergic mechanism, allowing them to learn where to obtain food reward in a T-maze runway. Their reward-learning-without-dopamine is revealed on a subsequent test day, when dopamine function is restored by L-dopa administration. Robinson et al. conclude that dopamine is not needed for normal learning about rewards, or for hedonic "liking" of rewards during learning, but rather specifically for a motivational "wanting" component of reward, such as incentive salience.

Animals↗

PubMed2004

Extinguishing the rewarding value of smoke cues: pharmacological and behavioral treatments.

The present study examined several pharmacological and behavioral treatments designed to promote extinction of the responses to rewarding cigarette smoke cues. Pharmacological treatments comprised nicotine skin patches (21 mg/24 hr) and the nicotinic acetylcholine receptor antagonist mecamylamine (10 mg/day), administered separately or in combination. Behavioral manipulations included switching to denicotinized cigarettes, to cigarettes having different menthol flavor, or to ventilated-filter (low tar and nicotine) cigarettes. Smokers were assigned to the various treatments for 2 weeks before they quit smoking. During weekly test sessions, subjects rated the rewarding effects of their usual brands of cigarettes or cigarettes with different menthol content (mentholated vs. nonmentholated). Over the 2-week treatment period, all pharmacological treatments reduced ratings of reward for the usual-brand test cigarettes. Switching to smoking denicotinized cigarettes for 2 weeks similarly decreased rewarding effects of the usual-brand test cigarettes. Subjects also strongly preferred cigarettes with the same menthol content to which they were accustomed. However, manipulating the menthol content of the cigarettes smoked during the 2 weeks of treatment had different effects, depending on whether smokers habitually smoked mentholated or nonmentholated cigarettes. For menthol smokers, removal of the menthol cue hampered extinction of reward ratings for the usual-brand (mentholated) test cigarette. For nonmenthol smokers, addition of the menthol cue did not affect the progress of extinction of nonmenthol smoke cues. These findings demonstrate the importance of sensory cues in determining subjective reward and show that the reward value of these cues can be altered by removal of nicotine from tobacco or by pharmacological manipulations that interfere with the reinforcing effects of nicotine.

Administration, Cutaneous↗

PubMed1992

The effects of amphetamine, apomorphine, SKF 38393, quinpirole and bromocriptine on responding for conditioned reward in rats.

The present study investigated the effects of the dopamine (DA) D1 selective agonist, SKF 38393, and the D2 selective agonists, quinpirole and bromocriptine, on responding for conditioned reward. The nonselective DA agonist apomorphine and the indirect agonist amphetamine, were also evaluated. Male rats (n = 302) were tested in a procedure consisting of three distinct phases. During the pre-exposure phase the rats were exposed to an operant chamber containing two levers; one lever produced a lights-off stimulus (3s) and the other a tone stimulus (3s). This was followed by 4 conditioning sessions during which the levers were removed and rats received pairings of the lights-off stimulus (80 per day) and food, presented according to a variable time 45s schedule. Two test sessions followed 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 pre-exposure. Drugs were administered prior to each test session. A saline group showed a higher ratio of responding for the lights-off stimulus than the tone stimulus, indicating that the lights-off stimulus had become a conditioned reward. Amphetamine (0.01-2.0mg/kg) and to a lesser extent, quinpirole (0.01-5.0mg/kg) and bromocriptine (0.05-10.0mg/kg) dose-dependently increased responding and specifically enhanced responding on the lever producing the conditioned reward. Apomorphine (0.1-5.0mg/kg) increased responding on both levers at higher doses but the conditioned reward effect was lost. SKF 38393 (0.1-10.0mg/kg) appeared to impair the acquisition of responding for conditioned reward. The results were interpreted as indicating that responding for conditioned reward may be dependent on a D1 receptor-mediated reward signal.

Journal Article↗

PubMed1982

Immediate reinforcement in delayed reward learning in pigeons.

Pigeons were trained on simultaneous red-green discrimination procedures with delayed reward and sequences of stimuli during the delay. In Experiment 1, three stimuli appeared during the 60-second intervals between the correct responses and reward, and the incorrect responses and nonreward. The stimulus that immediately followed a correct response also preceded nonreward, and the stimulus that followed an incorrect response preceded reward. These stimuli were 10 or .33 second in duration for different groups. Stimuli during the remainder of the delay interval differed following correct and incorrect responses. Group 10 initially persisted in the nonrewarded choice, but shifted to a preponderance of rewarded responses after further training. Group .33 rapidly acquired the correct response. Similar results were obtained in Experiment 2 where delay intervals consisted of opposite sequences of two stimuli of equal duration and total delays were 6, 20, or 60 seconds. Early in training, generalization of differential conditioned-reinforcing properties from the conditions preceding reward and nonreward to postchoice conditions had a greater effect relative to backchaining than it did later. It was concluded that delayed-reward learning is best analyzed in terms of the conditioned-reinforcing value of the patterns of cues that follow immediately after rewarded and nonrewarded responses.

Journal Article↗

PubMed2026

Effects of acute inflammatory challenge on anhedonia and social reward processing: A randomized controlled trial of endotoxin.

Anhedonia is a core feature of depression that reflects reward system dysfunction. Acute inflammatory challenge has been shown to induce transient anhedonia and reward processing deficits, but its effects on distinct components of social reward processes remain poorly understood. This randomized, double-blind, placebo-controlled study evaluated anhedonia and social reward responsivity following acute inflammatory challenge. Low-dose endotoxin (0.8 ng/kg body weight; n = 18) or placebo (same volume of 0.9% saline; n = 22) was administered to female adults (ages 25-44). Anhedonia (Snaith-Hamilton Pleasure Questionnaire) and blood samples for cytokine assessment were collected pre-infusion and 2 and 4 h post-infusion. Social reward motivation (wanting to engage in a social task) was assessed at a baseline eligibility visit and 2 h post-infusion. Sensitivity to positive social cues (attentional bias toward and recognition of happy faces) was assessed pre-infusion and 2 h post-infusion. Results showed that endotoxin increased anhedonic symptoms (p = .005) and decreased social motivation by 2 h post-infusion (p = .001); within the endotoxin condition, changes in both outcomes were associated with increases in TNF-α (p's < .04). A significant condition-by-time interaction for happy-face recognition (p = .011) was driven by increased accuracy in the placebo (p = .04) but not endotoxin (p = .43) condition. Endotoxin administration did not affect attentional bias toward happy faces. Findings suggest that acute inflammatory challenge induces anhedonia and reduces social motivation, with more limited effects on sensitivity to positive social cues, highlighting specific reward-related pathways through which immune activation may contribute to inflammation-associated depression. Future work could examine whether immune-related changes in social motivation contribute to motivational deficits in depression.

Humans↗

PubMed1980

Ratio scales of the reward values and punisher aversions of depressed undergraduates.

Two experiments (Ns = 116 and 154, respectively) tested theories that state that depressed people undervalue rewards or are overly averse to punishers. Rational zero-point scaling was used to obtain ratio scales of undergraduates' reward values and punisher aversions. As the theories predicted, depressed students consistently valued classmate praise about three- to six-tenths as highly as did nondepressed students; depressed females were 1.4 times more averse to all four punishers (classmate and professor criticism, incorrectness feedback, and monetary fine), while depressed males were 1.2 times more averse to the three intangible punishers. Contrary to the theories, depressed students consistently failed to undervalue the remaining three rewards (professor praise, money, and correctness feedback), and depressed males failed to be overly averse to a monetary fine. It was concluded that reward-value theories of depression received more narrow support than did the punisher-aversion theories. In addition, developmental theories of reward values were supported by the finding that studies from low social-status backgrounds valued the abstract rewards about seven-tenths as highly as did high status students.

Depressive Disorder↗

PubMed1991

Responses to reward in monkey dorsal and ventral striatum.

The sources of input and the behavioral effects of lesions and drug administration suggest that the striatum participates in motivational processes. We investigated the activity of single striatal neurons of monkeys in response to reward delivered for performing in a go-nogo task. A drop of liquid was given each time the animal correctly executed or withheld an arm movement in reaction to a visual stimulus. Of 1593 neurons, 115 showed increased activity in response to delivery of liquid reward in both go and nogo trials. Responding neurons were predominantly located in dorsal and ventromedial parts of anterior putamen, in dorsal and ventral caudate, and in nucleus accumbens. They were twice as frequent in ventral as compared to dorsal striatal areas. Responses occurred at a median latency of 337 ms and lasted for 525 ms, with insignificant differences between dorsal and ventral striatum. Reward responses differed from activity recorded in the face area of posterior putamen which varied synchronously with individual mouth movements. Responses were directly related to delivery of primary liquid reward and not to auditory stimuli associated with it. Most of them also occurred when reward was delivered outside of the task. These results demonstrate that neurons of dorsal and particularly ventral striatum are involved in processing information concerning the attribution of primary reward.

Animals↗

PubMed1976

Modulation of reward and aversion processes in the rat diencephalon by neuroleptics: differential effects of clozapine and haloperidol.

The effects of clozapine and haloperidol on self-stimulation in rats were investigated in a shuttle-box that provides concurrent rate-independent indexes of the rewarding and aversive components of intracranial stimulation. The use of two concurrent measures of performance permits the differentiation of specific reward modulation effects from the variety of nonspecific performance decrements that these drugs may produce. Clozapine produced a dose-dependent reduction in reward that could be clearly dissociated from its nonspecific effects. In contrast, the apparent reduction in reward produced by haloperidol could not be dissociated from a nonspecific performance decrement. Consequently, the attenuation of self-stimulation produced by haloperidol does not indicate a direct role for dopamine in modulating reward. It is suggested that the attenuation of reward produced by neuroleptics reflects a reduction in noradrenergic transmission, whereas their nonspecific effects reflect their blockade of dopamine receptors.

Animals↗

PubMed1993

Dopamine D1 and D2 antagonists attenuate amphetamine-produced enhancement of responding for conditioned reward in rats.

It has been suggested that the dopamine D1 receptor may play an important role in reward. The present study was undertaken to investigate the roles of dopamine D1 and D2 receptor subtypes in responding for conditioned reward. This was done by examining the effects of the D1 antagonist SCH 23390 and the D2 antagonists pimozide and metoclopramide on amphetamine-produced enhancement of responding for conditioned reward. The procedure consisted of three distinct phases. During the pre-exposure phase 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 was calculated as a ratio of the number of responses made during the pre-exposure phase. A group receiving the vehicle during the test sessions showed a greater ratio of responding for the lights-off stimulus than the tone stimulus, indicating that the lights-off stimulus had become a conditioned reward. Amphetamine (0.1, 1.0, 2.0 and 5.0 mg/kg, IP, 5 min prior to test) specifically enhanced responding on the lever producing conditioned reward. SCH 23390 (5.0 and 10.0 micrograms/kg, SC, 2 h before test) and pimozide (0.1 and 0.2 mg/kg, IP, 4 h before test) dose-dependently shifted the peak in the amphetamine dose-response function to the right, indicating an attenuation of conditioned reward.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗

PubMed1990

Diazepam and decision making in the rat: negative evidence for reduced tolerance to reward delay.

A laboratory decision-making paradigm was developed in which changes in behavioural planning in response to delays in reward delivery could be studied in the rat. The problem given was to choose between three behavioural options, lever-pressing or running into one of two arms fitted to the experimental chamber, in order to obtain rewards (water). Basically, the animal received rewards with a certain probability when pressing the lever. At certain random intervals, reward delivery by lever-presses was stopped. To restart the system, the animal had to abandon lever-pressing and run out into one of the arms. The arm lengths could be varied, and a time-delay for restarting the system could be introduced into one of the arms. These manipulations changed the arm preference so that a long arm, or an arm with a time delay, was avoided. It was specifically investigated whether the benzodiazepine diazepam selectively lowered the tolerance to accept reward delay. Such an effect of benzodiazepines has previously been proposed. After diazepam 1 mg/kg, the number of lever-presses before running into an arm and number of behavioural interruptions were increased, and interpreted to show a deficit in information processing and/or decision making. No evidence for a selective effect of diazepam to reduce tolerance to reward delays could be detected.

Animals↗

PubMed1990

Weight of financial reward in the decision by medical students and experienced healthy volunteers to participate in clinical trials.

The aim of this survey was twofold: to assess the willingness of medical students to volunteer for clinical trials and to evaluate the weight of the financial reward and other general details as seen by healthy volunteers who had already participated in clinical trials. A specific questionnaire was given to each group to be answered anonymously. Among the medical students only 2.9% had already volunteered, 39.7% said that they would never participate, 24.7% would do it for scientific interest, 32.2% for scientific interest and financial reward, and 4.2% for the financial reward alone. In experienced volunteers, financial reward was the main reason to participate (90%) followed by curiosity (6.3%). The financial reward actually received was considered adequate compensation for the time and discomfort by most of the volunteers (83.7%). The information supplied by the research team and the arrangements made to treat any hazardous event were considered adequate (47.5%) or optimal (42.5%). Almost all the experienced volunteers (93.8%) answered positively when asked about participation in future studies. The results show that financial reward is a very important reason for healthy volunteers to participate in clinical trials.

Adult↗

PubMed2006

Intact discrimination reversal learning but slowed responding to reward-predictive cues after dopamine D1 and D2 receptor blockade in the nucleus accumbens of rats.

RATIONALE: The prediction error hypothesis of dopamine action states that dopamine signals are necessary for the brain to update the predictive significance of cues. Yet, little is known whether D1 or D2 receptor-mediated signals in the nucleus accumbens core (AcbC) are required to learn a reversal of the predictive significance of cues. OBJECTIVE: Here we examined the effects of a selective D1 or D2 receptor blockade in the AcbC on learning a reversal of previously acquired cue-reward magnitude contingencies. MATERIALS AND METHODS: Rats were trained on a reaction time (RT) task demanding conditioned lever release with discriminative visual cues signalling in advance the upcoming reward magnitude (one or five food pellets). After acquisition, RTs were guided by cue-associated reward magnitudes, i.e. RTs of responses were significantly shorter for expected high vs low reward. Thereafter, cue-reward magnitude contingencies were reversed. Reversal learning was tested for 12 daily sessions with intra-AcbC micro-infusions being given on sessions 1-6. Subjects received pre-trial infusions of the selective D1 or D2 receptor antagonists, SCH23390 (0.5, 2 microg per side) or raclopride (1, 4 microg per side), or vehicle (0.5 microl). RESULTS: Intra-AcbC infusion of SCH23390 (0.5, 2 microg) or raclopride (1, 4 microg) did not inhibit discrimination reversal learning, but the higher dose of each drug increased RTs of instrumental responses. CONCLUSIONS: In a visual discrimination task as used here, D1 and D2 receptor-mediated signals in the AcbC seem to be unnecessary in updating the reward-predictive significance of cues, rather, they serve to activate instrumental behaviour.

Animals↗

PubMed2006

Evaluation of reward processes in an animal model of depression.

RATIONALE: Anhedonia is a core symptom of major depression. Deficits in reward function, which underlie anhedonia, can be readily assessed in animals. Therefore, anhedonia may serve as an endophenotype for understanding the neural circuitry and molecular pathways underlying depression. OBJECTIVE: Surprisingly, there is scant knowledge regarding alterations in brain reward function after olfactory bulbectomy (OB), an animal model which results in a behavioural syndrome responsive to chronic antidepressant treatment. Therefore, the present studies aimed to assess reward function after bulbectomy. MATERIALS AND METHODS: The present study utilized sucrose preference, cocaine-induced hyperlocomotion and intra-cranial self-stimulation (ICSS) responding to examine reward processes in the OB model. RESULTS: Bulbectomized animals showed a marked preference (>90%) for 0.8% sucrose solution compared with water; similar to the preference exhibited by sham controls. Importantly, there were pronounced deficits in brain reward function, as assessed using ICSS, which lasted 8 days before returning to baseline levels. Furthermore, bulbectomized animals were hyper-responsive to the locomotor stimulating properties of an acute and a repeated cocaine regimen. However, no difference in ICSS facilitation was observed in response to an acute cocaine injection. CONCLUSIONS: Taken together, these results suggest that bulbectomized rats display alterations in brain reward function, but these changes are not long-lasting and thus, not amenable to investigating the effects of pharmacological interventions. However, given that OB animals are hypersensitive to drugs of abuse, bulbectomy may be an appropriate inducing factor for the development of animal models of co-morbid depression and drug dependence.

Animals↗

PubMed2000

Effects of the non-competitive NMDA-receptor antagonist memantine on morphine- and cocaine-induced potentiation of lateral hypothalamic brain stimulation reward.

RATIONALE: NMDA-receptor antagonists may be of potential therapeutic use in several states of disease. It has been reported that drugs like MK-801 can potentiate the rewarding effects of other drugs, which may complicate the therapeutic use of this class of drugs. However, since MK-801 appears to be an "atypical" drug in several respects, other NMDA-receptor antagonists may not share this effect of MK-801. OBJECTIVES: We tested the effects of memantine, a clinically used NMDA-receptor antagonist, in a paradigm that has previously shown the reward-potentiating effects of MK-801 to see if this drug would yield qualitatively comparable results. METHODS: The effects of memantine on morphine- and cocaine-induced potentiation of brain stimulation reward were examined, using the rate-free curve-shift paradigm. RESULTS: Low doses of morphine (2.5 mg/kg) and cocaine (5 mg/kg) produced moderate decreases in the reward threshold frequency reflected in moderate leftward shifts of the function relating response rate to stimulation frequency. These effects were not altered by co-administration of an intermediate dose of memantine (5 mg/kg), but maximum response rate was significantly increased by these drug combinations. Higher doses of morphine (7.5 mg/kg) and cocaine (10 mg/kg) had stronger effects on the rate-frequency function and reward threshold. These effects were enhanced by co-administration of a high dose of memantine (10 mg/kg), while the effects on maximum response rate were less pronounced. CONCLUSIONS: These results demonstrate that fairly high doses of memantine and morphine or cocaine have to be combined in order to observe an enhancement of the latter drugs' potentiation of brain stimulation reward. In this respect, memantine differs markedly from MK-801, another non-competitive NMDA-receptor antagonist which has been shown to interact with morphine and cocaine at very low doses.

Analgesics, Opioid↗

PubMed1997

Enhanced stimulus-reward learning by intra-amygdala administration of a D3 dopamine receptor agonist.

The amygdala is considered to be a critical neural substrate underlying the formation of stimulus-reward associations, and is known to receive substantial innervation from dopaminergic neurons located within the ventral mesencephalon. However, relatively little is known about the function of the mesoamygdaloid dopamine projection in stimulus-reward learning. Recently, we have found post-session intra-amygdala microinjections of d-amphetamine to enhance appetitive Pavlovian conditioning as assessed in a discriminative approach task. In the present study, we have examined the effects of dopamine receptor agonists possessing relative selectivity for the D1, D2 and D3 receptor subtypes in order to examine more fully the role of the mesoamygdaloid dopamine projection in stimulus-reward learning. Thus, subjects were trained to associated an initially neutral stimulus (CS+) with 10% sucrose reward (US). A second, control stimulus (CS-) was also presented but never paired with sucrose reward. In order to measure specifically the conditioned response to CS+/CS- presentation, responding during CS and US presentations was measured separately. Immediately following each training session, subjects received bilateral intra-amygdala infusion of 0.1, 1 or 10 nmol/side of SKF-38393, quinpirole or 7-OH-DPAT. Infusions of SKF-38393 or quinpirole were without effect on CS+ approach. However, post-session intra-amygdala infusions of 7-OH-DPAT enhanced selectively CS+ approach in a dose-dependent fashion. No dose of any drug affected CS- approach, US behaviours, or measures of extraneous behaviour. Subsequent acquisition of a novel conditioned instrumental response was also unaffected. Thus, the present data indicate a selective involvement of the D3 dopamine receptor subtype in the modulation of stimulus-reward learning by the mesoamygdaloid dopamine projection.

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

PubMed1999

Differential effects of withdrawal from chronic amphetamine or fluoxetine administration on brain stimulation reward in the rat--interactions between the two drugs.

RATIONALE: Withdrawal from chronic amphetamine administration is characterized by deficits in reward that resemble some symptoms of depression. Nevertheless, the effects of long-term administration and withdrawal from other drugs, such as fluoxetine, that have the potential to elevate mood in depressed individuals have not been characterized. OBJECTIVES: The purpose of this study was to characterize the effects of withdrawal from chronic amphetamine or fluoxetine administration on central reward function. Furthermore, the effects of acute or chronic pretreatment with fluoxetine on responsiveness to an acute amphetamine challenge were examined to identify potential interactions between the two drugs. METHODS: A rate-independent discrete-trial threshold procedure was used to characterize self-stimulation behavior in rats prepared with bipolar electrodes in the medial forebrain bundle. RESULTS: Elevations in intracranial self-stimulation (ICSS) thresholds, reflecting a decrease in the reward value of the stimulation, were associated with withdrawal from various chronic amphetamine treatment regimens (1-5 mg/kg, three injections per day for 1, 2, 4 or 6 days). The magnitude and duration of threshold elevations were proportional to the duration and dose of amphetamine treatment prior to withdrawal. In contrast, no alterations in ICSS thresholds were associated with withdrawal from chronic fluoxetine treatment (5 mg/kg/day for 15 days). While neither acute nor chronic administration of fluoxetine alone altered ICSS thresholds, chronic pretreatment with fluoxetine blocked the threshold-lowering effect of acute amphetamine administration (4 mg/kg), but acute pretreatment did not. Amphetamine-induced decreases in response latency, a measure of motor performance, were not affected by either chronic or acute fluoxetine pretreatment. CONCLUSIONS: The results of these experiments suggest that chronic fluoxetine treatment may induce adaptive changes in serotonergic transmission that, in themselves, do not alter the function of central reward processes, but may alter the ability of amphetamine to potentiate ICSS reward. In addition, the lack of change in ICSS thresholds during withdrawal from the chronic fluoxetine treatment regimen used suggests that withdrawal from all mood-altering drugs may not necessarily produce changes in central reward functions.

Amphetamine↗