Search bioRxiv⌕ Search

Biology subjects

Eisenegger, C.

Publications and source records attributed to Eisenegger, C..

5 recordsLinked to original sources

Effects of dopamine and opioid receptor antagonism on the neural processing of social and non-social rewards

Rewards are a broad category of stimuli inducing approach behavior to aid survival. Extensive evidence from animal research has shown that wanting (the motivation to pursue a reward) and liking (the pleasure associated with its consumption) are mostly regulated by dopaminergic and opioidergic activity in dedicated brain areas. However, less is known about the neuroanatomy of dopaminergic and opioidergic regulation of reward processing in humans, especially when considering different types of rewards (i.e., social and non-social). To fill this gap of knowledge, we combined dopaminergic and opioidergic antagonism (via amisulpride and naltrexone administration) with functional neuroimaging to investigate the neurochemical and neuroanatomical bases of wanting and liking of matched non-social (food) and social (interpersonal touch) rewards, using a randomized, between-subject, placebo-controlled, double-blind design. While at the behavioral level no drug effect was observed, brain activity was modulated by the administered compounds. In particular, opioid antagonism, compared to placebo, was associated with reduced activity in the medial orbitofrontal cortex during consumption of the most valued social and non-social rewards. Dopamine antagonism, however, had no clear effects on brain activity in response to rewards anticipation. These findings provide insights into the neurobiology of human reward processing and suggest a similar opioidergic regulation of the neural responses to social and non-social reward consumption.

neuroscience↗

Blocking D2/D3 dopamine receptors increases volatility of beliefs when we learn to trust others

The ability to flexibly adjust beliefs about other people is crucial for human social functioning. Dopamine has been proposed to regulate the precision of beliefs, but direct behavioural evidence of this is lacking. We investigated how a relatively high dose of the selective D2/D3 dopamine receptor antagonist sulpiride impacts learning about other peoples prosocial attitudes in a repeated trust game. Using a Bayesian model of belief updating, we show that sulpiride increased the volatility of beliefs, which led to higher precision-weights on prediction errors. This effect was entirely driven by participants with genetically conferring higher dopamine availability (Taq1a polymorphism). Higher precision weights were reflected in higher reciprocal behaviour in the repeated trust game but not in single-round trust games. This finding suggests that antipsychotic medication might acutely reduce rigidity of pathological beliefs.

neuroscience↗

Effects of dopamine D2 and opioid receptor antagonism on the trade-off between model-based and model-free behavior in healthy volunteers

Our daily behaviour requires a flexible arbitration between actions we do out of habit and actions that are directed towards a specific goal. Drugs that target opioid and dopamine receptors are notorious for inducing maladaptive habitual drug consumption, yet how the opioidergic and dopaminergic neurotransmitter systems contribute to the arbitration between habitual and goal-directed behaviour is poorly understood. By combining pharmacological challenges with a well-established decision-making task and a novel computational model, we show that the administration of the D2 dopamine receptor antagonist amisulpride led to an increase in goal-directed or model-based relative to habitual or model-free behaviour, whereas the non-selective opioid receptor antagonist naltrexone had no appreciable effect. These findings highlight the distinct functional contributions of dopamine and opioid receptors to goal-directed and habitual behaviour and support the notion that D2 receptor antagonists promote stabilisation of goal-relevant information.

neuroscience↗

A causal role for estradiol in human reinforcement learning

The sex hormone estrogen is hypothesized to play a key role in human cognition via its interactions with the dopaminergic system. Work in rodents has shown that estrogens most potent form, estradiol, impacts striatal dopamine functioning predominately via increased D1-receptor signalling, while human work has suggested that high estradiol levels are associated with altered reward sensitivity. Here, we addressed two fundamental questions: 1) whether estradiol causally alters reward sensitivity in men, and 2) whether this effect of estradiol is moderated by individual variation in polymorphisms of dopaminergic genes. To test this, we performed a double-blind placebo-controlled administration study in which hundred men received either a single dose of estradiol (2 mg) or placebo. We found that estradiol administration increased reward sensitivity, which was moderated by baseline dopamine. This was observed in choice behaviour and increased learning rates. These results confirm a causal role of estradiol in reinforcement learning in men that is moderated by the striatal dopaminergic pathway.

neuroscience↗

Dopaminergic and opioidergic regulation of implicit and explicit wanting and liking of social and nonsocial rewards

The observation of animal hedonic orofacial and behavioral reactions has played a fundamental role for the identification of a dopaminergic motivational, and an opioidergic hedonic component of reward. Translation to humans remains difficult, however, as human research has struggled to adopt a similar operationalization of reward. Here, we investigated the neurochemical basis of hedonic facial and behavioral reactions to different types of rewards in healthy adult volunteers, by pharmacologically reducing dopaminergic and opiodergic receptor-specific action. Subjective ratings, physical effort, and facial reactions to matched primary social (affective touch) and nonsocial (food) rewards were assessed. Both drugs resulted in reduced physical effort and increased negative facial reactions during reward anticipation, but only opioidergic manipulation caused reduced positive facial reactions during reward consumption. This suggest that facial reactions during anticipated and experienced pleasure rely on partly different neurochemical systems, providing novel evidence in support of existing theoretical models of reward.

neuroscience↗