Reinforcement learning theory powerfully characterizes how we learn to benefit ourselves. In this theory, prediction errors-the difference between a predicted and actual outcome of a choice-drive learning. However, we do not operate in a social vacuum. To behave prosocially we must learn the consequences of our actions for other people. Empathy, the ability to vicariously experience and understand the affect of others, is hypothesized to be a critical facilitator of prosocial behaviors, but the link between empathy and prosocial behavior is still unclear. During functional magnetic resonance imaging (fMRI) participants chose between different stimuli that were probabilistically associated with rewards for themselves (self), another person (prosocial), or no one (control). Using computational modeling, we show that people can learn to obtain rewards for others but do so more slowly than when learning to obtain rewards for themselves. fMRI revealed that activity in a posterior portion of the subgenual anterior cingulate cortex/basal forebrain (sgACC) drives learning only when we are acting in a prosocial context and signals a prosocial prediction error conforming to classical principles of reinforcement learning theory. However, there is also substantial variability in the neural and behavioral efficiency of prosocial learning, which is predicted by trait empathy. More empathic people learn more quickly when benefitting others, and their sgACC response is the most selective for prosocial learning. We thus reveal a computational mechanism driving prosocial learning in humans. This framework could provide insights into atypical prosocial behavior in those with disorders of social cognition.reinforcement learning theory | prosocial behavior | empathy | reward | subgenual anterior cingulate cortex P rosocial behaviors, namely, social behaviors or actions intended to benefit others, are a fundamental but poorly understood aspect of social interaction (1). To behave prosocially, animals need to learn about the consequences that their actions can have for others. In reinforcement learning theory (RLT), prediction errors (PEs)-differences between expected and actual outcomesdrive learning (2). RLT provides a powerful framework for understanding how animals learn to obtain rewards for themselves (3). However, the processes by which animals learn to make choices that benefit others are unknown. Here we use RLT to characterize prosocial learning, combining functional magnetic resonance imaging (fMRI) and detailed computational modeling of behavior.Studies using economic games, moral judgments, or charity donation tasks have consistently reported activity in the ventral striatum, posterior regions of the subgenual cingulate cortex/basal forebrain (hereinafter referred to as sgACC), dorsal anterior cingulate cortex (dACC), and dorsolateral prefrontal cortex (DLPFC) during prosocial behavior (4-7). Each of these regions receives input from midbrain dopaminergic neurons (8), and these cortical regions all project to the ventral ...

Anxiety is characterized by altered responses under uncertain conditions, but the precise mechanism by which uncertainty changes the behaviour of anxious individuals is unclear. Here we probe the computational basis of learning under uncertainty in healthy individuals and individuals with a mix of mood and anxiety disorders. Participants chose between four competing slot machines with fluctuating, reward/punishment outcomes during safety and stress. We predicted that anxious individuals under stress would learn faster about punishments, and exhibit choices that were more affected by them, formalising our predictions as parameters in reinforcement-learning accounts of behaviour. Overall, data suggest that anxious individuals are quicker to update their behaviour in response to negative outcomes (i.e. increased punishment learning-rates). When treating anxiety, it may therefore be more fruitful to encourage anxious individuals to integrate information over longer horizons when bad things happen, rather than try to blunt responses to negative outcomes.

Recently, evidence for endemically low statistical power has cast neuroscience findings into doubt. If low statistical power plagues neuroscience, then this reduces confidence in the reported effects. However, if statistical power is not uniformly low, then such blanket mistrust might not be warranted. Here, we provide a different perspective on this issue, analyzing data from an influential study reporting a median power of 21% across 49 meta-analyses (Button et al., 2013). We demonstrate, using Gaussian mixture modeling, that the sample of 730 studies included in that analysis comprises several subcomponents so the use of a single summary statistic is insufficient to characterize the nature of the distribution. We find that statistical power is extremely low for studies included in meta-analyses that reported a null result and that it varies substantially across subfields of neuroscience, with particularly low power in candidate gene association studies. Therefore, whereas power in neuroscience remains a critical issue, the notion that studies are systematically underpowered is not the full story: low power is far from a universal problem.SIGNIFICANCE STATEMENT Recently, researchers across the biomedical and psychological sciences have become concerned with the reliability of results. One marker for reliability is statistical power: the probability of finding a statistically significant result given that the effect exists. Previous evidence suggests that statistical power is low across the field of neuroscience. Our results present a more comprehensive picture of statistical power in neuroscience: on average, studies are indeed underpowered—some very seriously so—but many studies show acceptable or even exemplary statistical power. We show that this heterogeneity in statistical power is common across most subfields in neuroscience. This new, more nuanced picture of statistical power in neuroscience could affect not only scientific understanding, but potentially policy and funding decisions for neuroscience research.

Computational modelling has been used to address: (1) the variety of symptoms observed in schizophrenia using abstract models of behavior (e.g. Bayesian models - top-down descriptive models of psychopathology); (2) the causes of these symptoms using biologically realistic models involving abnormal neuromodulation and/or receptor imbalance (e.g. connectionist and neural networks - bottom-up realistic models of neural processes). These different levels of analysis have been used to answer different questions (i.e. understanding behavioral vs. neurobiological anomalies) about the nature of the disorder. As such, these computational studies have mostly supported diverging hypotheses of schizophrenia's pathophysiology, resulting in a literature that is not always expanding coherently. Some of these hypotheses are however ripe for revision using novel empirical evidence. Here we present a review that first synthesizes the literature of computational modelling for schizophrenia and psychotic symptoms into categories supporting the dopamine, glutamate, GABA, dysconnection and Bayesian inference hypotheses respectively. Secondly, we compare model predictions against the accumulated empirical evidence and finally we identify specific hypotheses that have been left relatively under-investigated.