Coordinatore | UNIVERSITAET ZUERICH
Organization address
address: Raemistrasse 71 contact info |
Nazionalità Coordinatore | Switzerland [CH] |
Totale costo | 179˙101 € |
EC contributo | 179˙101 € |
Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | FP7-PEOPLE-2010-IIF |
Funding Scheme | MC-IIF |
Anno di inizio | 2011 |
Periodo (anno-mese-giorno) | 2011-06-01 - 2013-05-31 |
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UNIVERSITAET ZUERICH
Organization address
address: Raemistrasse 71 contact info |
CH (ZURICH) | coordinator | 179˙101.60 |
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'This project combines computational modeling, electroencephalography (EEG), functional magnetic resonance imaging (fMRI) and neuropharmacology to investigate the modulation of synaptic plasticity by dopamine during learning about both social and reward-based information. The purpose of the project is to evaluate biologically and computationally interpretable models for obtaining quantitative indices of synaptic plasticity during learning using both EEG and fMRI recording methods. To this aim, we apply a learning paradigm that combines both social and reward-based cues to guide behaviour. Following behavioural assessment, this paradigm will be used in pharmacological EEG and fMRI studies of healthy volunteers, employing a double-blind, placebo-controlled between-subject design with dopaminergic agents. Joint EEG and fMRI recordings will be obtained and analysed using state of the art modeling techniques, including novel approaches that embed hierarchical Bayesian learning models into nonlinear dynamic causal models. Specifically, we will test whether the models can quantify drug-induced changes in synaptic plasticity that occur as a function of trial-wise learning variables, such as reward prediction errors. Finally, we will use recent advances in model-based decoding to test whether our models can detect which pharmacological manipulation took place in any given subject. If these models prove to be mechanistically interpretable, this research could pave the way for future development of non-invasive, model-based measures of neurotransmitter regulation of synaptic plasticity in patients with psychiatric disorders.'
Scientists routinely measure dynamic changes in brain function through non-invasive recording techniques. A new EU-funded study developed a mathematical model to evaluate brain changes through simple behavioural measures.
The ability to measure changes in neural connectivity (synaptic plasticity) with tests of learning and to evaluate pharmacological effects on that would be of inestimable value. It would usher in a new era in treatment of nervous system disorders, including psychiatric ones.
EU-funded scientists set out to make it happen through work on the project 'Dopaminergic modulation of plasticity during social learning' (DOPAMINE&PLASTICITY). Researchers combined the use of behavioural paradigms, non-invasive recordings, genetics and computational modelling to extract quantitative measures of synaptic change.
The learning paradigm integrated social and reward-based cues to guide behaviour. This increased understanding of how people make decisions, how they integrate hidden cues about others' intentions and decide to follow or ignore them. Such information is valuable on a fundamental basis and in diagnosis and treatment of diseases such as autism spectrum disorder.
Electroencephalogram (EEG) and functional magnetic resonance imaging (fMRI) studies in healthy volunteers evaluated gross changes in brain activity. Dopamine is an important central nervous system neurotransmitter. The over-arching goal is to develop models that can quantify drug-induced changes in synaptic plasticity as a function of learning variables.
Researchers conducted the behavioural assessment in an fMRI study of healthy individuals and followed this with model development. They also carried out a genetic analysis combined with a model-based characterisation of neural mechanisms in such a task.
Together with modelling studies, outcomes suggest that dopamine-dependent mechanisms similar to those active during reinforcement learning may also operate during social learning. If true, social learning studies could benefit from application of the plethora of reward-learning studies carried out in animal models.
The pharmacological EEG and fMRI study will begin in the next few months. The team will assess the performance of the developed models. If they can detect which specific pharmacological intervention occurred in any given patient and even enable precise detection of functional dopamine receptor status, the study will pave the way to non-invasive, model-based measures of neurotransmitter regulation of synaptic plasticity. Outcomes would boost fundamental understanding while aiding diagnosis and therapy development in patients with deficits in social cognition such as autism spectrum disorder.