Seminars
September 2024
Prosocial Learning and Motivation across the Lifespan
Patricia Lockwood· University of Birmingham, UK
Recorded
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.
Video · 35 minCognitionComputational NeuroscienceSeries: British Association for Cognitive Neuroscience BACN
May 2021
Learning to perceive with new sensory signals
Marko Nardini· Durham University
Wed, May 19 · 13:00 UTC · Online
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.
May 2020
Cortical plasticity
Mriganka Sur· MIT Department of Brain and Cognitive Sciences
Thu, May 21 · 10:00 UTC · Online
Plasticity shapes the brain during development, and mechanisms of plasticity continue into adulthood to enable learning and memory. Nearly all brain functions are influenced by past events, reinforcing the view that the confluence of plasticity and computation in the same circuit elements is a core component of biological intelligence. My laboratory studies plasticity in the cerebral cortex during development, and plasticity during behaviour that is manifest as cortical dynamics. I will describe how cortical plasticity is implemented by learning rules that involve not only Hebbian changes and synaptic scaling but also dendritic renormalization. By using advanced techniques such as optical measurements of single-synapse function and structure in identified neurons in awake behaving mice, we have recently demonstrated locally coordinated plasticity in dendrites whereby specific synapses are strengthened and adjacent synapses with complementary features are weakened. Together, these changes cooperatively implement functional plasticity in neurons. Such plasticity relies on the dynamics of activity-dependent molecules within and between synapses. Alongside, it is increasingly clear that risk genes associated with neurodevelopmental disorders disproportionately target molecules of plasticity. Deficits in renormalization contribute fundamentally to dysfunctional neuronal circuits and computations, and may be a unifying mechanistic feature of these disorders.
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