Dopamine enhances expectation of pleasure in humans.
Ontology highlight
ABSTRACT:
SUBMITTER: Sharot T
PROVIDER: S-EPMC2801060 | biostudies-literature | 2009 Dec
REPOSITORIES: biostudies-literature
Publications
Dopamine enhances expectation of pleasure in humans.
Sharot Tali T Shiner Tamara T Brown Annemarie C AC Fan Judy J Dolan Raymond J RJ
Current biology : CB 20091112 24
Human action is strongly influenced by expectations of pleasure. Making decisions, ranging from which products to buy to which job offer to accept, requires an estimation of how good (or bad) the likely outcomes will make us feel [1]. Yet, little is known about the biological basis of subjective estimations of future hedonic reactions. Here, we show that administration of a drug that enhances dopaminergic function (dihydroxy-L-phenylalanine; L-DOPA) during the imaginative construction of positiv ...[more]
Similar Datasets
Project description:When predicting financial profits, relationship outcomes, longevity, or professional success, people habitually underestimate the likelihood of future negative events. This well-known bias, termed unrealistic optimism, is observed across age, culture, and species, and has a significant societal impact on domains ranging from financial markets to health and well being. However, it is unknown how neuromodulatory systems impact on the generation of optimistically biased beliefs. This question assumes great importance in light of evidence that common neuropsychiatric disorders, such as depression, are characterized by pessimism. Here, we show that administration of a drug that enhances dopaminergic function (dihydroxy-L-phenylalanine; L-DOPA) increases an optimism bias. This effect is due to L-DOPA impairing the ability to update belief in response to undesirable information about the future. These findings provide the first evidence that the neuromodulator dopamine impacts on belief formation by reducing negative expectations regarding the future.
| S-EPMC3424419 | biostudies-literature
Project description:Dopamine (DA) transmission in the nucleus accumbens (NAc) facilitates cue-reward associations and appetitive action. Reward-related accumbal DA release dynamics are traditionally ascribed to ventral tegmental area (VTA) DA neurons. Activation of VTA to NAc DA signaling is thought to reinforce action and transfer reward-related information to predictive cues, allowing cues to guide behavior and elicit dopaminergic activity. Here, we use optogenetics to control DA neuron activity and voltammetry to simultaneously record accumbal DA release in order to quantify how reinforcer-evoked dopaminergic activity shapes conditioned mesolimbic DA transmission. We find that cues predicting access to DA neuron self-stimulation elicit conditioned responding and NAc DA release. However, cue-evoked DA release does not reflect the cost or magnitude of DA neuron activation. Accordingly, conditioned accumbal DA release selectively tracks the expected availability of DA-neuron-mediated reinforcement. This work provides insight into how mesolimbic DA transmission drives and encodes appetitive action.
| S-EPMC6481661 | biostudies-literature
Project description:Prolonged mesolimbic dopamine concentration changes have been detected during spatial navigation, but little is known about the conditions that engender this signaling profile or how it develops with learning. To address this, we monitored dopamine concentration changes in the nucleus accumbens core of rats throughout acquisition and performance of an instrumental action sequence task. Prolonged dopamine concentration changes were detected that ramped up as rats executed each action sequence and declined after earned reward collection. With learning, dopamine concentration began to rise increasingly earlier in the execution of the sequence and ultimately backpropagated away from stereotyped sequence actions, becoming only transiently elevated by the most distal and unexpected reward predictor. Action sequence-related dopamine signaling was reactivated in well-trained rats if they became disengaged in the task and in response to an unexpected change in the value, but not identity of the earned reward. Throughout training and test, dopamine signaling correlated with sequence performance. These results suggest that action sequences can engender a prolonged mode of dopamine signaling in the nucleus accumbens core and that such signaling relates to elements of the motivation underlying sequence execution and is dynamic with learning, overtraining and violations in reward expectation.
| S-EPMC4751524 | biostudies-literature
Project description:Many animals use cues from another animal's gaze to help distinguish friend from foe. In humans, the direction of someone's gaze provides insight into their focus of interest and state of mind and there is increasing evidence linking abnormal gaze behaviors to clinical conditions such as schizophrenia and autism. This fundamental role of another's gaze is buoyed by the discovery of specific brain areas dedicated to encoding directions of gaze in faces. Surprisingly, however, very little is known about how others' direction of gaze is interpreted. Here we apply a Bayesian framework that has been successfully applied to sensory and motor domains to show that humans have a prior expectation that other people's gaze is directed toward them. This expectation dominates perception when there is high uncertainty, such as at night or when the other person is wearing sunglasses. We presented participants with synthetic faces viewed under high and low levels of uncertainty and manipulated the faces by adding noise to the eyes. Then, we asked the participants to judge relative gaze directions. We found that all participants systematically perceived the noisy gaze as being directed more toward them. This suggests that the adult nervous system internally represents a prior for gaze and highlights the importance of experience in developing our interpretation of another's gaze.
| S-EPMC3918857 | biostudies-other
Project description:The response to drugs of abuse is affected by expectation, which is modulated in part by dopamine (DA), which encodes for a reward prediction error. Here we assessed the effect of expectation on methylphenidate (MP)-induced striatal DA changes in 23 participants with an active cocaine use disorder (CUD) and 23 healthy controls (HC) using [11C]raclopride and PET both after placebo (PL) and after MP (0.5 mg/kg, i.v.). Brain dopamine D2 and D3 receptor availability (D2R: non-displaceable binding potential (BPND)) was measured under four conditions in randomized order: (1) expecting PL/receiving PL, (2) expecting PL/receiving MP, (3) expecting MP/receiving PL, and (4) expecting MP/receiving MP. Expecting MP increased pulse rate compared to expecting PL. Receiving MP decreased D2R in striatum compared to PL, indicating MP-induced striatal DA release, and this effect was significantly blunted in CUD versus HC consistent with prior findings of decreased striatal dopamine responses both in active and detoxified CUD. There was a group × challenge × expectation effect in caudate and midbrain, with expectation of MP increasing MP-induced DA release in HC but not in CUD, and expectation of PL showing a trend to increase MP-induced DA release in CUD but not in HC. These results are consistent with the role of DA in reward prediction error in the human brain: decreasing DA signaling when rewards are less than expected (blunted DA increases to MP in CUD) and increasing them when greater than expected (for PL in CUD reflecting conditioned responses to injection). Our findings also document disruption of the expectation of drug effects in dopamine signaling in participants with CUD compared to non-addicted individuals.
| S-EPMC6377670 | biostudies-literature
Project description:Converging evidence from both human neuroimaging and animal studies has supported a model of mesolimbic processing underlying reward learning behaviors, based on the computation of reward prediction errors. However, competing evidence supports human dopamine signaling in the basal ganglia as also contributing to the generation of higher order learning heuristics. Here, we present data from a large (N = 81, 18-30yo), multi-modal neuroimaging study using simultaneously acquired task fMRI, affording temporal resolution of reward system function, and PET imaging with [11C]Raclopride (RAC), assessing striatal dopamine (DA) D2/3 receptor binding, during performance of a probabilistic reward learning task. Both fMRI activation and PET DA measures showed ventral striatum involvement for signaling rewards. However, greater DA release was uniquely associated with learning strategies (i.e., learning rates) that were more task-optimal within the best fitting reinforcement learning model. This DA response was associated with BOLD activation of a network of regions including anterior cingulate cortex, medial prefrontal cortex, thalamus and posterior parietal cortex, primarily during expectation, rather than prediction error, task epochs. Together, these data provide novel, human in vivo evidence that striatal dopaminergic signaling interacts with a network of cortical regions to generate task-optimal learning strategies, rather than representing reward outcomes in isolation.
| S-EPMC9983071 | biostudies-literature
Project description:Disordered dopamine neurotransmission is implicated in mediating impulsiveness across a range of behaviors and disorders including addiction, compulsive gambling, attention-deficit/hyperactivity disorder, and dopamine dysregulation syndrome. Whereas existing theories of dopamine function highlight mechanisms based on aberrant reward learning or behavioral disinhibition, they do not offer an adequate account of the pathological hypersensitivity to temporal delay that forms a crucial behavioral phenotype seen in these disorders. Here we provide evidence that a role for dopamine in controlling the relationship between the timing of future rewards and their subjective value can bridge this explanatory gap. Using an intertemporal choice task, we demonstrate that pharmacologically enhancing dopamine activity increases impulsivity by enhancing the diminutive influence of increasing delay on reward value (temporal discounting) and its corresponding neural representation in the striatum. This leads to a state of excessive discounting of temporally distant, relative to sooner, rewards. Thus our findings reveal a novel mechanism by which dopamine influences human decision-making that can account for behavioral aberrations associated with a hyperfunctioning dopamine system.
| S-EPMC3059485 | biostudies-literature
Project description:Egalitarian motives form a powerful force in promoting prosocial behavior and enabling large-scale cooperation in the human species [1]. At the neural level, there is substantial, albeit correlational, evidence suggesting a link between dopamine and such behavior [2, 3]. However, important questions remain about the specific role of dopamine in setting or modulating behavioral sensitivity to prosocial concerns. Here, using a combination of pharmacological tools and economic games, we provide critical evidence for a causal involvement of dopamine in human egalitarian tendencies. Specifically, using the brain penetrant catechol-O-methyl transferase (COMT) inhibitor tolcapone [4, 5], we investigated the causal relationship between dopaminergic mechanisms and two prosocial concerns at the core of a number of widely used economic games: (1) the extent to which individuals directly value the material payoffs of others, i.e., generosity, and (2) the extent to which they are averse to differences between their own payoffs and those of others, i.e., inequity. We found that dopaminergic augmentation via COMT inhibition increased egalitarian tendencies in participants who played an extended version of the dictator game [6]. Strikingly, computational modeling of choice behavior [7] revealed that tolcapone exerted selective effects on inequity aversion, and not on other computational components such as the extent to which individuals directly value the material payoffs of others. Together, these data shed light on the causal relationship between neurochemical systems and human prosocial behavior and have potential implications for our understanding of the complex array of social impairments accompanying neuropsychiatric disorders involving dopaminergic dysregulation.
| S-EPMC4627633 | biostudies-literature
Project description:Placebo responses are primarily mediated via two neuropsychological mechanisms: patients' expectation towards the benefit of a treatment and associative learning processes. Immune functions, like other physiological responses, can be modulated through behavioral conditioning. However, it is unknown whether learned immune responses are affected by the number of re-expositions to the conditioned stimulus (CS) during evocation. Moreover, it is unclear whether immune functions can also be modulated through mere verbally induced expectation. In the experiments reported here, we investigated in healthy male volunteers with an established model of learned immunosuppression whether a single re-exposition to the CS is able to induce a behaviorally conditioned immunosuppression. This conditioned immunosuppression is reflected through a significantly decreased interleukin (IL)-2 production by anti-CD3 stimulated peripheral blood mononuclear cells. Our data revealed that in contrast to four CS re-expositions (control group n = 15; experimental group n = 17), a single CS re-exposition was not sufficient to significantly suppress IL-2 production (control group n = 9, experimental group n = 10). Furthermore, we could demonstrate that mere expectation of taking an immunosuppressant did not cause an immunosuppressive response (n = 8-9 per expectation condition). Together, these findings extend our knowledge about the kinetics and mechanisms of placebo-induced immunosuppression and provide therewith information for designing conditioning protocols, which might be employed as a supportive therapy in clinical settings.
| S-EPMC3504052 | biostudies-literature
Project description:BackgroundWe used positron emission tomography imaging with [11C]raclopride to examine the effects of consumption of alcohol or placebo beverage by participants with alcohol use disorder (AUD) compared with healthy participants with and without family history of AUD. We sought to assess dopamine release following alcohol exposure in relation to AUD risk.MethodsThree groups were enrolled: participants with AUD (n = 15) and healthy participants with family history negative (n = 34) or positive (n = 16) for AUD. Participants consumed a placebo (n = 65) or alcohol (n = 63) beverage in counterbalanced order before positron emission tomography scanning (128 scans). Binding potential (BPND) in the two drink conditions and the percent change in BPND between conditions were evaluated across striatal subregions. Subjective effects of beverage consumption were rated. Effects of group, drink order, and sex were evaluated.ResultsAlcohol resulted in greater dopamine release than did placebo in the ventral striatum (p < .001). There were no main effects of group, drink order, or sex on ventral striatum BPND or percent change in BPND. However, there was a drink order-by-group interaction (p = .02) whereby family history-positive participants who received placebo first had both lower placebo BPND and less difference between placebo and alcohol BPND than all other groups, consistent with expectation of alcohol powerfully evoking dopamine release in this group. Subjective responses showed the same order-by-group interaction.ConclusionsHyper-responsivity of the dopaminergic system in family history-positive participants to expectation of alcohol may contribute to the expression of familial risk for AUD.
| S-EPMC6953614 | biostudies-literature