A Snapshot seminar hosted by the School of Physiology, Pharmacology and Neuroscience.
Abstract: Cognitive flexibility, the ability to update one’s behaviour in response to changes in the environment, is impaired in many psychiatric and neurological disorders including schizophrenia, obsessive-compulsive disorder, and Parkinson’s disease. Current treatments for such disorders do not improve cognitive symptoms, and in the case of Parkinson’s disease, cognitive inflexibility is a side effect of the dopamine replacement therapy. One frequently used test of cognitive flexibility is reversal learning, which requires subjects to use trial and error to update responding and maximise their rewards in response to unsignalled changes of task rules. The brain circuitry underpinning this function is conserved across species, and information gained from rodent experiments could increase our understanding of the neural mechanisms of cognitive flexibility and its impairment in human disorders. In this talk, I will describe touchscreen-based reversal-learning paradigms for rats and mice that were inspired by neuropsychological tasks and test batteries. This has allowed us to explore the neural, psychological, and pharmacological mechanisms of reversal learning, with a particular focus on dopamine signalling at the D2-like receptors. We have found strong behavioural and computational evidence suggesting that dopamine D2-receptor agonists at high doses block learning from negative feedback in our tasks, with little or no impact on learning from positive feedback. Recent and on-going projects explore the brain circuitry, receptor subtypes, and intracellular signalling mechanisms involved in this effect. This work could ultimately improve current drug treatment or identify novel drug targets for the treatment of psychiatric and neurological disorders characterised by cognitive inflexibility.
After the talk there will be coffee and biscuits in the tearoom