Seminars

2024 BACN Early-Career Prize Lecture Many of our decisions affect other people. Our choices can decelerate climate change, stop the spread of infectious diseases, and directly help or harm others. Prosocial behaviours – decisions that help others – could contribute to reducing the impact of these challenges, yet their computational and neural mechanisms remain poorly understood. I will present recent work that examines prosocial motivation, how willing we are to incur costs to help others, prosocial learning, how we learn from the outcomes of our choices when they affect other people, and prosocial preferences, our self-reports of helping others. Throughout the talk, I will outline the possible computational and neural bases of these behaviours, and how they may differ from young adulthood to old age.

The last decade has seen a burgeoning interest in studying the neural and computational mechanisms that underpin social learning (learning from others). Many findings support the view that learning from other people is underpinned by the same, ‘domain-general’, mechanisms underpinning learning from non-social stimuli. Despite this, the idea that humans possess social-specific learning mechanisms - adaptive specializations moulded by natural selection to cope with the pressures of group living - persists. In this talk I explore the persistence of this idea. First, I present dissociations between social and non-social learning - patterns of data which are difficult to explain under the domain-general thesis and which therefore support the idea that we have evolved special mechanisms for social learning. Subsequently, I argue that most studies that have dissociated social and non-social learning have employed paradigms in which social information comprises a secondary, additional, source of information that can be used to supplement learning from non-social stimuli. Thus, in most extant paradigms, social and non-social learning differ both in terms of social nature (social or non-social) and status (primary or secondary). I conclude that status is an important driver of apparent differences between social and non-social learning. When we account for differences in status, we see that social and non-social learning share common (dopamine-mediated) mechanisms.

Human society operates on large-scale cooperation and shared norms of fairness. However, individual differences in cooperation and incentives to free-riding on others’ cooperation make large-scale cooperation fragile and can lead to reduced social-welfare. Deciphering the neural codes representing potential rewards/costs for self and others is crucial for understanding social decision-making and cooperation. I will first talk about how we integrate computational modeling with functional magnetic resonance imaging to investigate the neural representation of social value and the modulation by oxytocin, a nine-amino acid neuropeptide, in participants evaluating monetary allocations to self and other (self-other allocations). Then I will introduce our recent studies examining the neurobiological mechanisms underlying intergroup decision-making using hyper-scanning, and share with you how we alter intergroup decisions using psychological manipulations and pharmacological challenge. Finally, I will share with you our on-going project that reveals how individual cooperation spreads through human social networks. Our results help to better understand the neurocomputational mechanism underlying interpersonal and intergroup decision-making.

I will begin by describing recent research taking a new, model-based approach to perceptual development. This approach uncovers fundamental changes in information processing underlying the protracted development of perception, action, and decision-making in childhood. For example, integration of multiple sensory estimates via reliability-weighted averaging – widely used by adults to improve perception – is often not seen until surprisingly late into childhood, as assessed by both behaviour and neural representations. This approach forms the basis for a newer question: the scope for the nervous system to deploy useful computations (e.g. reliability-weighted averaging) to optimise perception and action using newly-learned sensory signals provided by technology. Our initial model system is augmenting visual depth perception with devices translating distance into auditory or vibro-tactile signals. This problem has immediate applications to people with partial vision loss, but the broader question concerns our scope to use technology to tune in to any signal not available to our native biological receptors. I will describe initial progress on this problem, and our approach to operationalising what it might mean to adopt a new signal comparably to a native sense. This will include testing for its integration (weighted averaging) alongside the native senses, assessing the level at which this integration happens in the brain, and measuring the degree of ‘automaticity’ with which new signals are used, compared with native perception.

Humans spend a lifetime learning, storing and refining a repertoire of motor memories. However, it is unknown what principle underlies the way our continuous stream of sensori-motor experience is segmented into separate memories and how we adapt and use this growing repertoire. Here we develop a principled theory of motor learning based on the key insight that memory creation, updating, and expression are all controlled by a single computation – contextual inference. Unlike dominant theories of single-context learning, our repertoire-learning model accounts for key features of motor learning that had no unified explanation and predicts novel phenomena, which we confirm experimentally. These results suggest that contextual inference is the key principle underlying how a diverse set of experiences is reflected in motor behavior.