Representation Of Reward Value Research Articles

Representation of Anticipated Rewards and Punishments in the Human Brain.

Subjective value is a core concept in neuroeconomics, serving as the basis for decision making. Despite the extensive literature on the neural encoding of subjective reward value in humans, the neural representation of punishment value remains relatively understudied. This review synthesizes current knowledge on the neural representation of reward value, including methodologies, involved brain regions, and the concept of common currency representation of diverse reward types in decision-making and learning processes. We then critically examine existing research on the neural representation of punishment value, highlighting conceptual and methodological challenges in human studies and insights gained from animal research. Finally, we explore how individual differences in reward and punishment processing may be linked to various mental illnesses, with a focus on stress-related psychopathologies. This review advocates for the integration of both rewards and punishments within value-based decision-making and learning frameworks, leveraging insights from cross-species studies and utilizing ecological gamified paradigms to reflect real-life scenarios.

Optogenetic inhibition of the orbitofrontal cortex disrupts inhibitory control during stop-change performance in male rats.

Historically, the orbitofrontal cortex (OFC) has been implicated in a variety of behaviors ranging from reversal learning and inhibitory control to more complex representations of reward value and task space. While modern interpretations of the OFC's function have focused on a role in outcome evaluation, these cognitive processes often require an organism to inhibit a maladaptive response or strategy. Single unit recordings from the OFC in rats performing a stop-change task show that the OFC responds strongly to STOP trials. To investigate the role that the OFC plays in stop-change performance we expressed halorhodopsin (eNpHR3.0) in excitatory neurons in the OFC and tested rats on the stop-change task. Previous work suggests that the OFC differentiates between STOP trials based on trial sequence (i.e., gS trials: STOP trials preceded by a GO versus sS trials: STOP trials preceded by a STOP). We found that yellow light activation of the eNpHR3.0 expressing neurons significantly decreased accuracy only on STOP trials that followed GO trials (gS trials). Further, optogenetic inhibition of OFC speeded reaction times on error trials. This suggests that the OFC plays a role in inhibitory control processes, and that this role needs to be accounted for in modern interpretations of OFC function.Significance Statement The orbitofrontal cortex (OFC) is a highly interconnected brain region thought to be essential for healthy cognitive function. Historically, research has implicated the OFC in the inhibition of inappropriate actions, however, more recent work has focused on its role in guiding value-based decision making. Using a modified version of a canonical inhibitory control task in combination with optogenetics, we show that while important for value-based decision making, disruption of excitatory neurons in the OFC impairs inhibitory control processes as well. This highlights the need for theoretical accounts of OFC function to accommodate its role in both types of cognitive processes.

Adaptor protein complex 2 in the orbitofrontal cortex predicts alcohol use disorder.

Alcohol use disorder (AUD) is a life-threatening disease characterized by compulsive drinking, cognitive deficits, and social impairment that continue despite negative consequences. The inability of individuals with AUD to regulate drinking may involve functional deficits in cortical areas that normally balance actions that have aspects of both reward and risk. Among these, the orbitofrontal cortex (OFC) is critically involved in goal-directed behavior and is thought to maintain a representation of reward value that guides decision making. In the present study, we analyzed post-mortem OFC brain samples collected from age- and sex-matched control subjects and those with AUD using proteomics, bioinformatics, machine learning, and reverse genetics approaches. Of the 4,500+ total unique proteins identified in the proteomics screen, there were 47 proteins that differed significantly by sex that were enriched in processes regulating extracellular matrix and axonal structure. Gene ontology enrichment analysis revealed that proteins differentially expressed in AUD cases were involved in synaptic and mitochondrial function, as well as transmembrane transporter activity. Alcohol-sensitive OFC proteins also mapped to abnormal social behaviors and social interactions. Machine learning analysis of the post-mortem OFC proteome revealed dysregulation of presynaptic (e.g., AP2A1) and mitochondrial proteins that predicted the occurrence and severity of AUD. Using a reverse genetics approach to validate a target protein, we found that prefrontal Ap2a1 expression significantly correlated with voluntary alcohol drinking in male and female genetically diverse mouse strains. Moreover, recombinant inbred strains that inherited the C57BL/6J allele at the Ap2a1 interval consumed higher amounts of alcohol than those that inherited the DBA/2J allele. Together, these findings highlight the impact of excessive alcohol consumption on the human OFC proteome and identify important cross-species cortical mechanisms and proteins that control drinking in individuals with AUD.

Pleasure, Reward Value, Prediction Error and Anhedonia.

In order to develop effective treatments for anhedonia we need to understand its underlying neurobiological mechanisms. Anhedonia is conceptually strongly linked to reward processing, which involves a variety of cognitive and neural operations. This chapter reviews the evidence for impairments in experiencing hedonic response (pleasure), reward valuation and reward learning based on outcomes (commonly conceptualised in terms of "reward prediction error"). Synthesising behavioural and neuroimaging findings, we examine case-control studies of patients with depression and schizophrenia, including those focusing specifically on anhedonia. Overall, there is reliable evidence that depression and schizophrenia are associated with disrupted reward processing. In contrast to the historical definition of anhedonia, there is surprisingly limited evidence for impairment in the ability to experience pleasure in depression and schizophrenia. There is some evidence that learning about reward and reward prediction error signals are impaired in depression and schizophrenia, but the literature is inconsistent. The strongest evidence is for impairments in the representation of reward value and how this is used to guide action. Future studies would benefit from focusing on impairments in reward processing specifically in anhedonic samples, including transdiagnostically, and from using designs separating different components of reward processing, formulating them in computational terms, and moving beyond cross-sectional designs to provide an assessment of causality.

Chemogenetic Inactivation of Orbitofrontal Cortex Decreases Cue-induced Reinstatement of Ethanol and Sucrose Seeking in Male and Female Wistar Rats.

The orbitofrontal cortex (OFC) encodes internal representations of outcomes and subjective value to facilitate flexible reward seeking. OFC activation is associated with drug seeking in both human subjects and animal models. OFC plays a role in alcohol use, but studies in animal models have produced conflicting results with some showing decreased seeking after OFC inactivation but others showing increased seeking or no changes. In part, this may be due to the different measures of alcohol seeking used (e.g., homecage drinking vs. operant seeking). We characterized the impact of transient inactivation of OFC (primarily lateral and, to a lesser extent, ventral subregions) using inhibitory hM4Di designer receptors exclusively activated by designer drugs (DREADDs). OFC neurons were transiently inhibited during 10% and 20% alcohol (ethanol, EtOH) and sucrose homecage consumption, fixed ratio (FR1) operant self-administration, and cue-induced reinstatement of either 10% EtOH or sucrose in male and female rats. OFC inactivation did not affect sucrose or EtOH consumption in the homecage, nor did it influence seeking or consumption under FR1 operant conditions. In contrast, OFC inactivation suppressed cued-induced reinstatement for both EtOH and sucrose in both male and female rats. Our results are aligned with previous work indicating a selective suppressive effect of OFC inactivation on reinstatement for alcohol and other drugs of abuse. They extend these findings to demonstrate no effect on homecage consumption or FR1 seeking as well as showing an impact of sucrose reinstatement. These data indicate that OFC plays a uniquely important role when reward seeking is driven by associations between external stimuli and internal representations of reward value, both for natural and drug rewards. They further implicate the OFC as a key structure driving relapse-associated seeking and potentially contributing to alcohol use disorder and other diseases of compulsive reward seeking.

The orbitofrontal cortex: reward, emotion and depression.

The orbitofrontal cortex in primates including humans is the key brain area in emotion, and in the representation of reward value and in non-reward, that is not obtaining an expected reward. Cortical processing before the orbitofrontal cortex is about the identity of stimuli, i.e. ‘what’ is present, and not about reward value. There is evidence that this holds for taste, visual, somatosensory and olfactory stimuli. The human medial orbitofrontal cortex represents many different types of reward, and the lateral orbitofrontal cortex represents non-reward and punishment. Not obtaining an expected reward can lead to sadness, and feeling depressed. The concept is advanced that an important brain region in depression is the orbitofrontal cortex, with depression related to over-responsiveness and over-connectedness of the non-reward-related lateral orbitofrontal cortex, and to under-responsiveness and under-connectivity of the reward-related medial orbitofrontal cortex. Evidence from large-scale voxel-level studies and supported by an activation study is described that provides support for this hypothesis. Increased functional connectivity of the lateral orbitofrontal cortex with brain areas that include the precuneus, posterior cingulate cortex and angular gyrus is found in patients with depression and is reduced towards the levels in controls when treated with medication. Decreased functional connectivity of the medial orbitofrontal cortex with medial temporal lobe areas involved in memory is found in patients with depression. Some treatments for depression may act by reducing activity or connectivity of the lateral orbitofrontal cortex. New treatments that increase the activity or connectivity of the medial orbitofrontal cortex may be useful for depression. These concepts, and that of increased activity in non-reward attractor networks, have potential for advancing our understanding and treatment of depression. The focus is on the orbitofrontal cortex in primates including humans, because of differences of operation of the orbitofrontal cortex, and indeed of reward systems, in rodents. Finally, the hypothesis is developed that the orbitofrontal cortex has a special role in emotion and decision-making in part because as a cortical area it can implement attractor networks useful in maintaining reward and emotional states online, and in decision-making.

Fidelity of the representation of value in decision-making.

The ability to make optimal decisions depends on evaluating the expected rewards associated with different potential actions. This process is critically dependent on the fidelity with which reward value information can be maintained in the nervous system. Here we directly probe the fidelity of value representation following a standard reinforcement learning task. The results demonstrate a previously-unrecognized bias in the representation of value: extreme reward values, both low and high, are stored significantly more accurately and precisely than intermediate rewards. The symmetry between low and high rewards pertained despite substantially higher frequency of exposure to high rewards, resulting from preferential exploitation of more rewarding options. The observed variation in fidelity of value representation retrospectively predicted performance on the reinforcement learning task, demonstrating that the bias in representation has an impact on decision-making. A second experiment in which one or other extreme-valued option was omitted from the learning sequence showed that representational fidelity is primarily determined by the relative position of an encoded value on the scale of rewards experienced during learning. Both variability and guessing decreased with the reduction in the number of options, consistent with allocation of a limited representational resource. These findings have implications for existing models of reward-based learning, which typically assume defectless representation of reward value.

Goal-Directed and Habit-Like Modulations of Stimulus Processing during Reinforcement Learning.

Recent research has shown that perceptual processing of stimuli previously associated with high-value rewards is automatically prioritized even when rewards are no longer available. It has been hypothesized that such reward-related modulation of stimulus salience is conceptually similar to an "attentional habit." Recording event-related potentials in humans during a reinforcement learning task, we show strong evidence in favor of this hypothesis. Resistance to outcome devaluation (the defining feature of a habit) was shown by the stimulus-locked P1 component, reflecting activity in the extrastriate visual cortex. Analysis at longer latencies revealed a positive component (corresponding to the P3b, from 550-700 ms) sensitive to outcome devaluation. Therefore, distinct spatiotemporal patterns of brain activity were observed corresponding to habitual and goal-directed processes. These results demonstrate that reinforcement learning engages both attentional habits and goal-directed processes in parallel. Consequences for brain and computational models of reinforcement learning are discussed.SIGNIFICANCE STATEMENT The human attentional network adapts to detect stimuli that predict important rewards. A recent hypothesis suggests that the visual cortex automatically prioritizes reward-related stimuli, driven by cached representations of reward value; that is, stimulus-response habits. Alternatively, the neural system may track the current value of the predicted outcome. Our results demonstrate for the first time that visual cortex activity is increased for reward-related stimuli even when the rewarding event is temporarily devalued. In contrast, longer-latency brain activity was specifically sensitive to transient changes in reward value. Therefore, we show that both habit-like attention and goal-directed processes occur in the same learning episode at different latencies. This result has important consequences for computational models of reinforcement learning.

Deficits in reinforcement learning but no link to apathy in patients with schizophrenia

Negative symptoms in schizophrenia have been linked to selective reinforcement learning deficits in the context of gains combined with intact loss-avoidance learning. Fundamental mechanisms of reinforcement learning and choice are prediction error signaling and the precise representation of reward value for future decisions. It is unclear which of these mechanisms contribute to the impairments in learning from positive outcomes observed in schizophrenia. A recent study suggested that patients with severe apathy symptoms show deficits in the representation of expected value. Considering the fundamental relevance for the understanding of these symptoms, we aimed to assess the stability of these findings across studies. Sixty-four patients with schizophrenia and 19 healthy control participants performed a probabilistic reward learning task. They had to associate stimuli with gain or loss-avoidance. In a transfer phase participants indicated valuation of the previously learned stimuli by choosing among them. Patients demonstrated an overall impairment in learning compared to healthy controls. No effects of apathy symptoms on task indices were observed. However, patients with schizophrenia learned better in the context of loss-avoidance than in the context of gain. Earlier findings were thus partially replicated. Further studies are needed to clarify the mechanistic link between negative symptoms and reinforcement learning.

Role of orbitofrontal cortex in reward sensitivity: evidence from human lesions

BackgroundAn emerging hypothesis from cognitive neuroscience is that the ventromedial prefrontal cortex (vmPFC) is central to the evaluation and expectation of reward. However, there is scant evidence that lesions in this region alter reward processing. Rather, patients with damage in vmPFC have shown many conflicting effects with respect to motivation and affect. We aimed to specifically examine incentivisation by reward after damage to human vmPFC. MethodsWe selected a group of 19 patients with highly focal medial frontal lesions, from a database of 453 patients with subarachnoid haemorrhage, and 32 age-matched healthy controls. We directly tested for sensitivity to incentives using eye movements. Lesions included anterior cingulate, vmPFC, and medial orbitofrontal cortex. The task required participants to make saccadic eye movements to a target while avoiding a distractor, to obtain speed-related rewards. Crucially, before each eye movement, participants heard a reward cue indicating the maximum reward available. We examined the effect of the incentive cue on subsequent saccade velocity, and how this motivational effect was altered by medial frontal damage. FindingsIn healthy people, mean peak saccadic velocity was modulated by the incentive (from 458 degrees per s [SE 15] to 489 [17], p=0·0011), allowing a parametric measure of reward sensitivity. As a group, patients with medial frontal damage had significantly reduced effects of reward on invigorating saccadic velocity (from 443 degrees per s [SE 16] to 459 [19], p=0·038) and autonomic (pupil) responses (z-score traces significantly differed after 653 ms, p<0·05) compared with controls. However at the individual level, some patients showed the opposite effect, with abnormally strong incentivisation effects (3 SD above controls). Voxel-based lesion mapping demonstrated that within the lesion group, increased sensitivity to rewards correlated with damage to vmPFC subregions (144 voxels=1·15 cm3 whole-brain corrected). Lesions to vmPFC were also associated with clinical apathy (p=0·027 in region of interest) suggesting that apathy associated with prefrontal damage is reduced by vmPFC damage. InterpretationThis study found that, although medial frontal lesions could generally reduce reward sensitivity, damage to key subregions paradoxically were protective of this effect. Changes in reward sensitivity caused by altered representation of reward value might be a central link between various facets of behavioural changes seen after medial frontal damage. The results suggest a direct, mechanistic role for prefrontal reward computation in clinical motivation syndromes. FundingWellcome Trust.

Altered cingulo-striatal function underlies reward drive deficits in schizophrenia

Amotivation in schizophrenia is assumed to involve dysfunctional dopaminergic signaling of reward prediction or anticipation. It is unclear, however, whether the translation of neural representation of reward value to behavioral drive is affected in schizophrenia. In order to examine how abnormal neural processing of response valuation and initiation affects incentive motivation in schizophrenia, we conducted functional MRI using a deterministic reinforcement learning task with variable intervals of contingency reversals in 20 clinically stable patients with schizophrenia and 20 healthy controls. Behaviorally, the advantage of positive over negative reinforcer in reinforcement-related responsiveness was not observed in patients. Patients showed altered response valuation and initiation-related striatal activity and deficient rostro-ventral anterior cingulate cortex activation during reward approach initiation. Among these neural abnormalities, rostro-ventral anterior cingulate cortex activation was correlated with positive reinforcement-related responsiveness in controls and social anhedonia and social amotivation subdomain scores in patients. Our findings indicate that the central role of the anterior cingulate cortex is in translating action value into driving force of action, and underscore the role of the cingulo-striatal network in amotivation in schizophrenia.

Dopaminergic Circuitry and Risk/Reward Decision Making: Implications for Schizophrenia

Abnormal reinforcement learning and representations of reward value are present in schizophrenia, and these impairments can manifest as deficits in risk/reward decision making. These abnormalities may be due in part to dopaminergic dysfunction within cortico-limbic-striatal circuitry. Evidence from studies with laboratory animal have revealed that normal DA activity within different nodes of these circuits is critical for mediating dissociable processes that can refine decision biases. Moreover, both phasic and tonic dopamine transmission appear to play separate yet complementary roles in these processes. Tonic dopamine release within the prefrontal cortex and nucleus accumbens, serves as a "running rate-meter" of reward and reflects contextual information such as reward uncertainty and overt choice behavior. On the other hand, manipulations of outcome-related phasic dopamine bursts and dips suggest these signals provide rapid feedback to allow for quick adjustments in choice as reward contingencies change. The lateral habenula is a key input to the DA system that phasic signals is necessary for expressing subjective decision biases; as suppression of activity within this nucleus leads to catastrophic impairments in decision making and random patterns of choice behavior. As schizophrenia is characterized by impairments in using positive and negative feedback to appropriately guide decision making, these findings suggest that these deficits in these processes may be mediated, at least in part, by abnormalities in both tonic and phasic dopamine transmission.

Functional Disconnection of the Orbitofrontal Cortex and Basolateral Amygdala Impairs Acquisition of a Rat Gambling Task and Disrupts Animals' Ability to Alter Decision-Making Behavior after Reinforcer Devaluation

An inability to adjust choice preferences in response to changes in reward value may underlie key symptoms of many psychiatric disorders, including chemical and behavioral addictions. We developed the rat gambling task (rGT) to investigate the neurobiology underlying complex decision-making processes. As in the Iowa Gambling task, the optimal strategy is to avoid choosing larger, riskier rewards and to instead favor options associated with smaller rewards but less loss and, ultimately, greater long-term gain. Given the demonstrated importance of the orbitofrontal cortex (OFC) and basolateral amygdala (BLA) in acquisition of the rGT and Iowa Gambling task, we used a contralateral disconnection lesion procedure to assess whether functional connectivity between these regions is necessary for optimal decision-making. Disrupting the OFC-BLA pathway retarded acquisition of the rGT. Devaluing the reinforcer by inducing sensory-specific satiety altered decision-making in control groups. In contrast, disconnected rats did not update their choice preference following reward devaluation, either when the devalued reward was still delivered or when animals needed to rely on stored representations of reward value (i.e., during extinction). However, all rats exhibited decreased premature responding and slower response latencies after satiety manipulations. Hence, disconnecting the OFC and BLA did not affect general behavioral changes caused by reduced motivation, but instead prevented alterations in the value of a specific reward from contributing appropriately to cost-benefit decision-making. These results highlight the role of the OFC-BLA pathway in the decision-making process and suggest that communication between these areas is vital for the appropriate assessment of reward value to influence choice.

A biased activation theory of the cognitive and attentional modulation of emotion.

Cognition can influence emotion by biasing neural activity in the first cortical region in which the reward value and subjective pleasantness of stimuli is made explicit in the representation, the orbitofrontal cortex (OFC). The same effect occurs in a second cortical tier for emotion, the anterior cingulate cortex (ACC). Similar effects are found for selective attention, to for example the pleasantness vs. the intensity of stimuli, which modulates representations of reward value and affect in the orbitofrontal and anterior cingulate cortices. The mechanisms for the effects of cognition and attention on emotion are top-down biased competition and top-down biased activation. Affective and mood states can in turn influence memory and perception, by backprojected biasing influences. Emotion-related decision systems operate to choose between gene-specified rewards such as taste, touch, and beauty. Reasoning processes capable of planning ahead with multiple steps held in working memory in the explicit system can allow the gene-specified rewards not to be selected, or to be deferred. The stochastic, noisy, dynamics of decision-making systems in the brain may influence whether decisions are made by the selfish-gene-specified reward emotion system, or by the cognitive reasoning system that explicitly calculates reward values that are in the interests of the individual, the phenotype.

Action controls dopaminergic enhancement of reward representations

Dopamine is widely observed to signal anticipation of future rewards and thus thought to be a key contributor to affectively charged decision making. However, the experiments supporting this view have not dissociated rewards from the actions that lead to, or are occasioned by, them. Here, we manipulated dopamine pharmacologically and examined the effect on a task that explicitly dissociates action and reward value. We show that dopamine enhanced the neural representation of rewarding actions, without significantly affecting the representation of reward value as such. Thus, increasing dopamine levels with levodopa selectively boosted striatal and substantia nigra/ventral tegmental representations associated with actions leading to reward, but not with actions leading to the avoidance of punishment. These findings highlight a key role for dopamine in the generation of appetitively motivated actions.

Changes in reward-related signals in the rat nucleus accumbens measured by in vivo oxygen amperometry are consistent with fMRI BOLD responses in man

Real-time in vivo oxygen amperometry, a technique that allows measurement of regional brain tissue oxygen (O2) has been previously shown to bear relationship to the BOLD signal measured with functional magnetic resonance imaging (fMRI) protocols. In the present study, O2 amperometry was applied to the study of reward processing in the rat nucleus accumbens to validate the technique with a behavioural process known to cause robust signals in human neuroimaging studies. After acquisition of a cued-lever pressing task a robust increase in O2 tissue levels was observed in the nucleus accumbens specifically following a correct lever press to the rewarded cue. This O2 signal was modulated by cue reversal but not lever reversal, by differences in reward magnitudes and by the motivational state of the animal consistent with previous reports of the role of the nucleus accumbens in both the anticipation and representation of reward value. Moreover, this modulation by reward value was related more to the expected incentive value rather than the hedonic value of reward, also consistent with previous reports of accumbens coding of “wanting” of reward. Altogether, these results show striking similarities to those obtained in human fMRI studies suggesting the use of oxygen amperometry as a valid surrogate for fMRI in animals performing cognitive tasks, and a powerful approach to bridge between different techniques of measurement of brain function.

Dopaminergic and prefrontal contributions to reward-based learning and outcome monitoring during child development and aging.

In many instances, children and older adults show similar difficulties in reward-based learning and outcome monitoring. These impairments are most pronounced in situations in which reward is uncertain (e.g., probabilistic reward schedules) and if outcome information is ambiguous (e.g., the relative value of outcomes has to be learned). Furthermore, whereas children show a greater sensitivity to external outcome information, older adults focus less on a rapid differentiation of rewarding outcomes. In this article, we review evidence for the idea that these phenomenologically similar impairments in learning and outcome monitoring in children and older adults can be attributed to deficits in different underlying neurophysiological mechanisms. We propose that in older adults learning impairments are the result of reduced dopaminergic projections to the ventromedial prefrontal cortex, which lead to less differentiated representations of reward value. In contrast, in children, impairments in learning can be primarily attributed to deficits in executive control, which may be due to a protracted development of the dorsal medial and lateral prefrontal cortices. We think that this framework maps well onto recent neurophysiological models of reward processing and is plausible from a broader developmental perspective.

The relevance of reward pathways for schizophrenia

There has been a resurgence of interest in the field of reward processing in schizophrenia in recent years, aided by insights from functional neuroimaging. We examine how disturbances in reward-related processes relate to the pathophysiology and symptomatology of this disorder. Behavioural and functional neuroimaging studies in psychosis demonstrate impairments in the representation of reward value and in reward-related learning and a failure to motivate behaviour for incentives. These impairments are linked to abnormal mesocorticolimbic and mesostriatal function. Abnormalities in reward processing offer insights into the symptomatology of schizophrenia and its underlying neurobiology. Further investigation is required into the specificity of these deficits to particular symptom expression and to what extent they are improved by antipsychotic treatment.

Dopamine in the prefrontal cortex regulates rats behavioral flexibility to changing reward value

Prefrontocortical dopamine (DA) plays an essential role in the representation of reward value and is implicated in behavioral flexibility. We here tested the effect of systemic and local blockade of DA D1- and D2-receptors in the medial prefrontal cortex (mPFC) and orbitofrontal cortex (OFC) by using an operant paradigm, where rats have to adjust their behavior to changing reward value. Rats were trained in a Skinner box, where different numbers of lever-presses for pellet-rewards were assigned to and switched between two levers. After rats commit to the efficient lever the lever-occupancy reversed and rats had to switch to the now efficient one. Rats were either intraperitoneally injected with the DA D1-receptor antagonist SCH23390 (40 μg/kg), the DA D2-receptor antagonist sulpiride (10 mg/kg), or phosphate buffered saline (PBS). Two other groups received bilateral local mPFC- or OFC-infusions of SCH23390, sulpiride (both 3 μg/0.5 μl), or PBS (0.5 μl) through previously implanted cannulae. After initial detection of reverse of lever-occupancy, systemic and local blockade of D1-receptors increased the number of switches back to the previously efficient lever, thus reducing the total number of reverses completed. D2-receptor blockade deteriorated this measure after local mPFC-infusion. Notably, initial detection of reverse of lever-occupancy was not affected. Blockade of DA receptors within the prefrontal cortex do not deteriorate the detection of changes in reward value, whereas maintenance of behavioral adaptation is disturbed. Interestingly, blockade of DA receptors in the mPFC and OFC had similar effects, i.e., these regions apparently act in a cooperative manner.

Delta EEG Activity in Left Orbitofrontal Cortex in Rats Related to Food Reward and Craving

The orbitofrontal cortex (OFC) is particularly important for the neural representation of reward value. Previous studies indicated that electroencephalogram (EEG) activity in the OFC was involved in drug administration and withdrawal. The present study investigated EEG activity in the OFC in rats during the development of food reward and craving. Two environments were used separately for control and food-related EEG recordings. In the food-related environment rats were first trained to eat chocolate peanuts; then they either had no access to this food, but could see and smell it (craving trials), or had free access to this food (reward trials). The EEG in the left OFC was recorded during these trials. We showed that, in the food-related environment the EEG activity peaking in the delta band (2-4 Hz) was significantly correlated with the stimulus, increasing during food reward and decreasing during food craving when compared with that in the control environment. Our data suggests that EEG activity in the OFC can be altered by food reward; moreover, delta rhythm in this region could be used as an index monitoring changed signal underlying this reward.