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PubMed1989

Brain dopamine and reward.

While the evidence is strong that dopamine plays some fundamental and special role in the rewarding effects of brain stimulation, psychomotor stimulants, opiates, and food, the exact nature of that role is not clear. One thing is clear: Dopamine is not the only reward transmitter, and dopaminergic neurons are not the final common path for all rewards. Dopamine antagonists and lesions of the dopamine systems appear to spare the rewarding effects of nucleus accumbens and frontal cortex brain stimulation (Simon et al 1979) and certainly spare the rewarding effects of apomorphine (Roberts & Vickers 1988). It is clear that reward circuitry is multisynaptic, and since dopamine cells do not send axons to each other or receive axons from each other, dopamine can at best serve as but a single link in this circuitry. If dopamine is not a final common path for all rewards, could it be an intermediate common path for most rewards? Some workers have argued against such a view, but at present they must do so on incomplete evidence. For example, Phillips (1984) has argued that there must be multiple reward systems, functionally independent and organized in parallel with one another. His primary evidence, however, is the fact that brain stimulation is rewarding at different levels of the nervous system. As we have seen in the case of midline mesencephalic stimulation, the location of the electrode tip in relation to the dopamine cells and fibers tells us little about the role of dopamine in brain stimulation reward. It seems clear that the ventral tegmental dopamine system plays a critical role in midline mesencephalic reward, despite the distance from the electrode tip to the dopamine cells where morphine causes its dopamine-dependent facilitory effects or to the dopamine terminals where low-dose neuroleptics presumably cause theirs. Until pharmacological challenge has been extended to the cases discussed by Phillips, we can only speculate as to the role of dopamine in each of those cases. In the cases where pharmacological challenge has been examined, only nucleus accumbens and frontal cortex have been found to have dopamine-independent reward sites. It is not consistent with the dopamine hypothesis that dopamine-independent reward sites should exist in these areas, since any reward signals carried to nucleus accumbens or frontal cortex by dopamine fibers would-unless we are to believe that reward "happens" at these sites-have to be carried to the next stage of the circuit by nondopaminergic fibers (there are no dopaminergic cell bodies in any of the dopamine terminal areas).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

A possible role of midbrain dopamine neurons in short- and long-term adaptation of saccades to position-reward mapping.

Dopamine (DA) neurons respond to sensory stimuli that predict reward. To understand how DA neurons acquire such ability, we trained monkeys on a one-direction-rewarded version of memory-guided saccade task (1DR) only when we recorded from single DA neurons. In 1DR, position-reward mapping was changed across blocks of trials. In the early stage of training of 1DR, DA neurons responded to reward delivery; in the later stages, they responded predominantly to the visual cue that predicted reward or no reward (reward predictor) differentially. We found that such a shift of activity from reward to reward predictor also occurred within a block of trials after position-reward mapping was altered. A main effect of long-term training was to accelerate the within-block reward-to-predictor shift of DA neuronal responses. The within-block shift appeared first in the intermediate stage, but was slow, and DA neurons often responded to the cue that indicated reward in the preceding block. In the advanced stage, the reward-to-predictor shift occurred quickly such that the DA neurons' responses to visual cues faithfully matched the current position-reward mapping. Changes in the DA neuronal responses co-varied with the reward-predictive differentiation of saccade latency both in short-term (within-block) and long-term adaptation. DA neurons' response to the fixation point also underwent long-term changes until it occurred predominantly in the first trial within a block. This might trigger a switch between the learned sets. These results suggest that midbrain DA neurons play an essential role in adapting oculomotor behavior to frequent switches in position-reward mapping.

Adaptation, Physiological↗
PubMed2003

Firing of nucleus accumbens neurons during the consummatory phase of a discriminative stimulus task depends on previous reward predictive cues.

The nucleus accumbens (NAc) plays an important role in both appetitive and consummatory behavior. To examine how NAc neurons encode information during reward consumption, we recorded the firing activity of rat NAc neurons during the performance of a discriminative stimulus task. In this task, the animal must make an operant response to an intermittently presented cue to obtain a sucrose reward delivered in a reward receptacle. Uncued entries to the receptacle were not rewarded. Both excitations and inhibitions during reward consumption were observed, but substantially more neurons were inhibited than excited. These excitations and inhibitions began when the animal entered the reward receptacle and ended when the animal exited the receptacle. Both excitations and inhibitions were much smaller or nonexistent when the animal made uncued entries into the reward receptacle. In one set of experiments, we randomly withheld the reward in some cued trials that would otherwise have been rewarded. Excitations and inhibitions were of similar magnitude whether or not the reward was delivered. This indicates that the sensory stimulus of reward does not drive these phasic responses; instead, the reward-associated responses may be driven by the conditioned stimuli associated with reward, or they may encode information about consummatory motor activity. Another population of NAc neurons was excited on exit from the reward receptacle. Many of these excitations persisted for tens of seconds after the receptacle exit and showed a significant inverse correlation with the rate of uncued operant responding. These findings are consistent with a contribution of NAc neurons to both reward consummatory and reward seeking behavior.

Action Potentials↗
PubMed2003

Reward-predicting activity of dopamine and caudate neurons--a possible mechanism of motivational control of saccadic eye movement.

Recent studies have suggested that the basal ganglia are related to motivational control of behavior. To study how motivational signals modulate motor signals in the basal ganglia, we examined activity of midbrain dopamine (DA) neurons and caudate (CD) projection neurons while monkeys were performing a one-direction-rewarded version (1DR) of memory-guided saccade task. The cue stimulus indicated the goal position for an upcoming saccade and the presence or absence of reward after the trial. Among four monkeys we studied, three were sensitive to reward such that saccade velocity was significantly higher in the rewarded trials than in the nonrewarded trials; one monkey was insensitive to reward. In the reward-sensitive monkeys, both DA and CD neurons responded differentially to reward-indicating and no-reward-indicating cues. Thus DA neurons responded with excitation to a reward-indicating cue and with inhibition to a no-reward-indicating cue. A group of CD neurons responded to the cue in their response fields (mostly contralateral) and the cue response was usually enhanced when it indicated reward. In the reward-insensitive monkey, DA neurons showed no response to the cue, while the cue responses of CD neurons were not modulated by reward. Many CD neurons in the reward-sensitive monkeys, but not the reward-insensitive monkey, showed precue activity. These results suggest that DA neurons, with their connection to CD neurons, modulate the spatially selective signals in CD neurons in the reward-predicting manner and CD neurons in turn modulate saccade parameters with their polysynaptic connections to the oculomotor brain stem.

Animals↗
PubMed2001

Behavioral reactions reflecting differential reward expectations in monkeys.

Learning theory emphasizes the importance of expectations in the control of instrumental action. This study investigated the variation of behavioral reactions toward different rewards as an expression of differential expectations of outcomes in primates. We employed several versions of two basic behavioral paradigms, the spatial delayed response task and the delayed reaction task. These tasks are commonly used in neurobiological studies of working memory, movement preparation, and event expectation involving the frontal cortex and basal ganglia. An initial visual instruction stimulus indicated to the animal which one of several food or liquid rewards would be delivered after each correct behavioral response, or whether or not a reward could be obtained. We measured the reaction times of the operantly conditioned arm movement necessary for obtaining the reward, and the durations of anticipatory licking prior to liquid reward delivery as a Pavlovian conditioned response. The results showed that both measures varied depending on the reward predicted by the initial instruction. Arm movements were performed with significantly shorter reaction times for foods or liquids that were more preferred by the animal than for less preferred ones. Still larger differences were observed between rewarded and unrewarded trials. An interesting effect was found in unrewarded trials, in which reaction times were significantly shorter when a highly preferred reward was delivered in the alternative rewarded trials of the same trial block as compared to a less preferred reward. Anticipatory licks preceding the reward were significantly longer when highly preferred rather than less preferred rewards, or no rewards, were predicted. These results demonstrate that behavioral reactions preceding rewards may vary depending on the predicted future reward and suggest that monkeys differentially expect particular outcomes in the presently investigated tasks.

Animals↗
PubMed2000

Reward processing in primate orbitofrontal cortex and basal ganglia.

This article reviews and interprets neuronal activities related to the expectation and delivery of reward in the primate orbitofrontal cortex, in comparison with slowly discharging neurons in the striatum (caudate, putamen and ventral striatum, including nucleus accumbens) and midbrain dopamine neurons. Orbitofrontal neurons showed three principal forms of reward-related activity during the performance of delayed response tasks, namely responses to reward-predicting instructions, activations during the expectation period immediately preceding reward and responses following reward. These activations discriminated between different rewards, often on the basis of the animals' preferences. Neurons in the striatum were also activated in relation to the expectation and detection of reward but in addition showed activities related to the preparation, initiation and execution of movements which reflected the expected reward. Dopamine neurons responded to rewards and reward-predicting stimuli, and coded an error in the prediction of reward. Thus, the investigated cortical and basal ganglia structures showed multiple, heterogeneous, partly simultaneous activations which were related to specific aspects of rewards. These activations may represent the neuronal substrates of rewards during learning and established behavioral performance. The processing of reward expectations suggests an access to central representations of rewards which may be used for the neuronal control of goaldirected behavior.

Animals↗
PubMed1986

Lateral hypothalamus neuron involvement in integration of natural and artificial rewards and cue signals.

Involvement of rat lateral hypothalamus (LHA) neurons in integration of motivation, reward, and learning processes was studied by recording single-neuron activity during cuetone discrimination, learning behavior to obtain glucose, or electrical rewarding intracranial self-stimulation (ICSS) of the posterior LHA. To relate the activity of an LHA neuron to glucose, ICSS, and anticipatory cues, the same licking task was used to obtain both rewards. Each neuron was tested with rewards alone and then with rewards signaled by cuetone stimuli (CTS), CTS1+ = 1,200 Hz for glucose, CTS2+ = 4,300 Hz for ICSS, and CTS- = 2,800 Hz for no reward. The activity of 318 neurons in the LHA was analyzed. Of these, 212 (66.7%) responded to one or both rewarding stimuli (glucose, 115; ICSS, 193). Usually, both rewards affected the same neuron in the same direction. Of 96 neurons that responded to both rewards, the responses of 72 (75%) were similar, i.e., either both excitatory or both inhibitory. When a tone was associated with glucose or ICSS reward, 81 of the 212 neurons that responded to either or both rewards and none of 106 neurons that failed to respond to either reward acquired a response to the respective CTS. Usually, the response to a tone was in the same direction as the reward response. Of 45 neurons that responded to both glucose and CTS1+, 38 (84.4%) were similar, and of 66 that responded to both ICSS and CTS2+, 47 (71.2%) were similar. The neural response to a tone was acquired rapidly after licking behavior was learned and was extinguished equally rapidly before licking stopped in extinction. The latency of the neural response to CTS1+ was 10-150 ms (58.7 +/- 40.9 ms, mean +/- SE, n = 31), and that of the first lick was 100-370 ms (204.8 +/- 59.1 ms, n = 31). The latency of neural responses to CTS2+ was 10-230 ms (68.3 +/- 53.5 ms, n = 33), and that of the first lick was 90-370 ms (212.4 +/- 58.5 ms, n = 33). There was no significant difference between the neural response latencies for the two cue tones nor between the lick latencies for the different rewards. Neurons inhibited by glucose or ICSS reward were distributed widely in the LHA, whereas most excited neurons were in the posterodorsal subarea; fewer were in the anteroventral subarea. Neurons responding to the CTS for glucose or ICSS were found more frequently in the posterior region.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2007

Parameters of variable reward distributions that affect risk sensitivity of honey bees.

We investigated risk sensitivity with harnessed honey bees in a proboscis-extension conditioning paradigm. We conditioned each subject to turn its head and extend its proboscis towards one of two presented odors; one odor was associated with a constant reward and the other with a variable reward that was either low or high, with probabilities P and (1-P), respectively. Reward values and probabilities were set so that the expected value of the variable alternative was equal to that of the constant one. We performed six experimental conditions in which variability was in reward volume and three conditions in which variability was in reward concentration. The experiments were designed to systematically test the effect of various parameters that describe the reward distributions on levels of risk sensitivity. Risk aversion was greatest when variability was in reward volume, and the variable distribution included zero rewards and had a high coefficient of variation (CV=s.d./mean). The variance itself did not affect risk sensitivity. Subjects were risk indifferent when the variable distribution did not include zero rewards, however these distributions were positively skewed. The independent effects of zero rewards and distribution skew remain to be tested. Subjects were risk indifferent in conditions where variability was in reward concentration, but concentration range was limited and these distributions did not include zero rewards and were skewed. We conclude that risk aversion to variability in reward amount is a robust phenomenon for some reward distributions. A systematic evaluation of the effect of various reward distribution parameters on choice behavior should complement functional and mechanistic approaches.

Analysis of Variance↗
PubMed2000

Effects of dopaminergic drugs on delayed reward as a measure of impulsive behavior in rats.

RATIONALE: Impulsive individuals exhibit an exaggerated preference for immediate rewards over delayed but larger rewards, perhaps because they value the delayed rewards less. Dopamine (DA) has been postulated to mediate the incentive value of rewards, thus it may also mediate the exaggerated preference for immediate rewards in impulsive individuals. In this paper, we investigate the effects of DA agonists and antagonists on the value of delayed versus immediate rewards. OBJECTIVES: The study had three main objectives: (1) to determine the effects of D1 and D2 type DA antagonists on the value of delayed rewards, (2) to determine the effect of the indirect DA agonist d-amphetamine on the value of delayed rewards, (3) to determine the sensitivity of the adjusting amount (AdjAmt) procedure to acute one-day changes in delay to reward, amount of reward, deprivation level and starting amount. METHODS: In the AdjAmt procedure, rats choose between an adjusting amount of water given immediately (adjusting alternative) and a constant 150 microliters water delayed by 4 s (standard alternative). The immediate amount of water is adjusted across trials until the rat chooses both alternatives with equal frequency (indifference point). The final adjusted amount is an indicator of the subjective value of the standard alternative. RESULTS: The D1/D2 antagonist flupenthixol (25, 50, and 100 micrograms/kg) and the D2 antagonist raclopride (40, 80, and 120 micrograms/kg), decreased the indifference points, whereas the D1 antagonist SCH 23390 (5, 10, and 20 micrograms/kg) did not affect the indifference point. All three DA antagonists slowed responding. The indirect DA agonist amphetamine (0.5, and 1.0 mg/kg) had effects opposite to those of the DA antagonists, it decreased choice latency, increased the number of trials completed and increased the indifference point. Decreasing the water deprivation level (6, 24, and 48 h) had no effect on the indifference points but slowed responding. Increasing the delay to reward (2, 4, and 8 s) and decreasing the amount of water available for choosing the standard alternative (300, 150, 75 microliters) decreased the indifference point. CONCLUSIONS: The results indicate that amphetamine increased the value of delayed rewards (decreased impulsivity) and that D2 but not D1 receptor antagonists decreased the value of delayed rewards (increased impulsivity). The procedure was sensitive to acute 1-day changes in delay and magnitude of reward.

Amphetamine↗
PubMed2005

Correspondence of cue activity to reward activity in the macaque orbitofrontal cortex.

It has been reported that neurons in the orbitofrontal cortex (OFC) respond to emotionally significant events such as reward-predicting cues and/or the reward itself. The responses to reward-predicting cues are considered to carry the information of the predicted reward. However, few studies have focused on the relationship of the neuronal activity during a cue period with that during a reward period. We can infer that the cue responses of OFC neurons are correlated to the reward responses if they carry the information of the predicted reward. In this study, we focused on neurons that showed responses during both the cue and reward periods, and compared the response characteristics between these periods. We found 94 of 369 OFC neurons showed significant responses during both the cue and reward periods, and 43 of which preserved their selectivity between these periods. Furthermore, population analysis showed that stronger cue responses corresponded to stronger reward responses, and stronger reward responses corresponded to stronger cue responses. These results suggest that individual neurons in the OFC associate visual information with reward information, and contribute to the prediction of future rewards by forming reward representations.

Animals↗
PubMed2004

Prediction error for free monetary reward in the human prefrontal cortex.

Making predictions about future rewards is an important ability for primates, and its neurophysiological mechanisms have been studied extensively. One important approach is to identify neural systems that process errors related to reward prediction (i.e., areas that register the occurrence of unpredicted rewards and the failure of expected rewards). In monkeys that have learned to predict appetitive rewards during reward-directed behaviors, dopamine neurons reliably signal both types of prediction error. The mechanisms in the human brain involved in processing prediction error for monetary rewards are not well understood. Furthermore, nothing is known of how such systems operate when rewards are not contingent on behavior. We used event-related fMRI to localize responses to both classes of prediction error. Subjects were able to predict a monetary reward or a nonreward on the basis of a prior visual cue. On occasional trials, cue-outcome contingencies were reversed (unpredicted rewards and failure of expected rewards). Subjects were not required to make decisions or actions. We compared each type of prediction error trial with its corresponding control trial in which the same prediction did not fail. Each type of prediction error evoked activity in a distinct frontotemporal circuit. Unexpected reward failure evoked activity in the temporal cortex and frontal pole (area 10). Unpredicted rewards evoked activity in the orbitofrontal cortex, the frontal pole, parahippocampal cortex, and cerebellum. Activity time-locked to prediction errors in frontotemporal circuits suggests that they are involved in encoding the associations between visual cues and monetary rewards in the human brain.

Basal Ganglia↗
PubMed2005

Development of a behavioral task measuring reward "wanting" and "liking" in rats.

It has been suggested that reward "wanting" and "liking" are mediated by separable brain systems. To facilitate neuropharmacological and neurophysiological research on this issue we developed a behavioral task with putative measures of reward "wanting" and "liking" available on a trial-by-trial basis. We were able to test whether our measures were sensitive to changes in thirsty rats' "wanting" and "liking" of liquid reward by manipulating its delay, taste and volume. We found that three of our putative "wanting" measures (anticipatory errors, reaction time and reward collection latency) were affected by upcoming reward delay and/or taste and our putative "liking" measure (post-reward licking) was sensitive to variations in reward taste and volume. To cross-validate our measures with previous pharmacological work we tested rats following acute, systemic administration of drug compounds that globally enhance serotonin and noradrenaline (imipramine), dopamine (GBR 12909) and opioid (morphine) function. Imipramine augmented the effects of delay and taste on reward "wanting", GBR 12909 attenuated the effects of delay on reward "wanting" and the effects of taste on reward "liking", and morphine reduced the effect of delay on a measure of reward "wanting". Since morphine failed to affect reward "liking" but has been previously found to enhance reward "liking" in taste reactivity tests, our measure requires further pharmacological validation. However, this task shows potential to assess the specific neural mechanisms that contribute to the impact of reward parameters on "wanting" and "liking".

Adrenergic Agents↗
PubMedDate not supplied

Opiate reward: sites and substrates.

Opiates appear to have rewarding actions at more than one locus in the brain. Studies of the effects of dopaminergic lesions and dopamine receptor blockade indicate that intravenous heroin self-administration depends importantly on a dopaminergic substrate. Mapping of effective injection sites for morphine-conditioned place preference establishes one site of rewarding action near the dopamine cell bodies of the ventral tegmental area (VTA). Studies of the complex interactions of opiates, neuroleptics, and brain stimulation reward confirm that reward-related VTA opioid actions are dopamine-dependent. Opioid injections into the nucleus accumbens (NAS) also facilitate brain stimulation reward and serve as rewards in their own right, though these actions have not yet been localized by identification of negative sites in surrounding regions. The relation of this putative reward site to the dopamine system is not yet clear. Suggestions that the lateral hypothalamus or periaqueductal gray contain opioid reward sites remain to be confirmed. While opioid injections into these sites can be rewarding, these rewarding effects have not been localized to these sites, and opiate injections into each of these areas are reported not to facilitate brain stimulation reward. Intravenous heroin self-administration is not disrupted by kainic acid lesions of the bed nucleus of the lateral hypothalamus. Thus only the VTA and the NAS are firmly established as sites of opiate rewarding actions. Recent reports suggest that the kappa-opioid dynorphin may also have central rewarding actions and central and peripheral aversive actions; the CA3 region of the hippocampus is a possible site of the rewarding action.

Animals↗
PubMed2005

Neural correlates of the proximity and quantity of anticipated food rewards in the ventral striatum of domestic chicks.

To identify the neuro-cognitive substrates of valuation and choice, we analysed the neural correlates of anticipated food rewards in the ventral striatum of freely behaving chicks. One-week-old chicks were trained in a color-discrimination task using four color cues (red, yellow, green and blue), each of which was associated with a different food reward. Choosing a red bead was immediately rewarded with a large amount of food, choosing a yellow bead resulted in an immediate-small food reward, and choosing a green bead resulted in a late-large food reward. We selected chicks that consistently chose a large and immediate food reward (red over yellow, and red over green), with the proximity of the food valued higher than the size of the food reward (yellow over green). Of the 47 neurons recorded from the ventral striatum of these chicks, 20 neurons selectively showed cue-period responses to cues associated with food rewards. Five of these 20 neurons responded differentially during the cue period according to the expected delay to reward, and were thus assumed to code for the proximity of the reward. Additionally, three other neurons responded to the quantity of the reward. Furthermore, in the post-operant delay period, many of these 20 neurons showed reward-related activities that were linked to the proximity or presence of the food reward. We therefore propose that impulsive choice and behavioral perseveration observed after lesions of the ventral striatum could be due to impaired anticipation of rewards in the cue and delay periods, respectively.

Animals↗
PubMed2005

Learning to like: a role for human orbitofrontal cortex in conditioned reward.

A great deal of human behavior and motivation is based on the intrinsic emotional significance of rewarding or aversive events, as well as on the associations formed between such emotional events and concurrent environmental stimuli. Recent functional neuroimaging studies have implicated the ventral striatum, orbitofrontal cortex (OFC), and amygdala in the representation of reward values and/or in the anticipation of rewarding events. Here, we use functional magnetic resonance imaging to compare brain activation during the presentation of reward with that during presentation of (conditioned) stimuli that have been paired previously with reward. Specifically, we aimed to investigate conditioned reward in the absence of explicit reward anticipation. Twenty-two healthy volunteers were scanned while monochrome visual patterns were incidentally associated with reward or negative feedback in the context of a simple card game. In the subsequent session, visual patterns, including the conditioned stimuli, were presented without reward or negative feedback, and the affective valence of these stimuli was assessed behaviorally. The presentation of reward compared with negative feedback activated the ventral striatum and OFC. Activation in the same OFC region was observed when, in the subsequent session, subjects passively viewed the stimuli that had been paired with reward, without the administration of reward and with subjects being essentially unaware of the conditioning manipulation. These findings suggest that the OFC in humans plays an important role in the representation of both rewarding stimuli and conditioned stimuli that have acquired reward value.

Adolescent↗
PubMed2005

Endocannabinoid signaling system and brain reward: emphasis on dopamine.

The brain's reward circuitry consists of an "in series" circuit of dopaminergic (DA) neurons in the ventral tegmental area (VTA), nucleus accumbens (Acb), and that portion of the medial forebrain bundle (MFB) which links the VTA and Acb. Drugs which enhance brain reward (and have derivative addictive potential) have common actions on this core DA reward system and on animal behaviors relating to its function. Such drugs enhance electrical brain-stimulation reward in this reward system; enhance neural firing and DA tone within it; produce conditioned place preference (CPP), a behavioral model of incentive motivation; are self-administered; and trigger reinstatement of drug-seeking behavior in animals extinguished from drug self-administration. Cannabinoids were long considered different from other reward-enhancing drugs in reward efficacy and in underlying neurobiological substrates activated. However, it is now clear that cannabinoids activate these brain reward processes and reward-related behaviors in similar fashion to other reward-enhancing drugs. This brief review discusses the roles that endogenous cannabinoids (especially activation of the CB1 receptor) may play within the core reward system, and concludes that while cannabinoids activate the reward pathways in a manner consistent with other reward-enhancing drugs, the neural mechanisms by which this occurs may differ.

Animals↗
PubMed1999

Relative reward preference in primate orbitofrontal cortex.

The orbital part of prefrontal cortex appears to be crucially involved in the motivational control of goal-directed behaviour. Patients with lesions of orbitofrontal cortex show impairments in making decisions about the expected outcome of actions. Monkeys with orbitofrontal lesions respond abnormally to changes in reward expectations and show altered reward preferences. As rewards constitute basic goals of behaviour, we investigated here how neurons in the orbitofrontal cortex of monkeys process information about liquid and food rewards in a typical frontal task, spatial delayed responding. The activity of orbitofrontal neurons increases in response to reward-predicting signals, during the expectation of rewards, and after the receipt of rewards. Neurons discriminate between different rewards, mainly irrespective of the spatial and visual features of reward-predicting stimuli and behavioural reactions. Most reward discriminations reflect the animals' relative preference among the available rewards, as expressed by their choice behaviour, rather than physical reward properties. Thus, neurons in the orbitofrontal cortex appear to process the motivational value of rewarding outcomes of voluntary action.

Animals↗
PubMed2003

Withdrawal from chronic phencyclidine treatment induces long-lasting depression in brain reward function.

Phencyclidine (PCP) is a drug of abuse that has rewarding and dysphoric effects in humans. The complex actions of PCP, and PCP withdrawal in particular, on brain reward function remain unclear. The purpose of the present study was to characterize the effects of withdrawal from acute and chronic PCP treatment on brain reward function in rats. A brain stimulation reward procedure was used to evaluate the effects of acute PCP injection (0, 5, or 10 mg/kg) or chronic PCP treatment (0, 10, 15, or 20 mg/kg/day for 14 days delivered via subcutaneous osmotic minipumps) on brain reward function. Withdrawal from acute administration of 5 and 10 mg/kg PCP produced a decrease in brain reward function as indicated by a sustained elevation in brain reward thresholds. When administered chronically, 10, 15, or 20 mg/kg/day PCP induced a progressive dose-dependent potentiation of brain stimulation reward, while cessation of the treatment resulted in significant elevations in reward thresholds reflecting diminished reward. Specifically, withdrawal from 15 or 20 mg/kg/day PCP induced a depression in brain reward function that lasted for the entire month of observation. These results indicate that prolonged continuous administration of high PCP doses facilitates brain stimulation reward, while withdrawal from acute high PCP doses or chronic PCP treatment results in a protracted depression of brain reward function that may be analogous to the dysphoric and anhedonic symptoms observed in PCP dependence, depression, and schizophrenia.

Animals↗