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Physiopathology of addiction
Pier Vincenzo Piazza
Neurogenesis and pathophysiology
Nora Abrous
Glia-neuron interactions
Stéphane Oliet
Motor system diseases
Gwendal Le Masson
Planar polarity and plasticity
Mireille Montcouquiol & Nathalie Sans
Endocannabinoids and Neuroadaptation
Giovanni Marsicano
Energy Balance and Obesity
Daniela Cota
Cortical Plasticity
Andreas Frick
Pathophysiology of declarative memory
Aline Marighetto
Neuronal circuits of associative learning
Cyril Herry
 

Team 'Cortical plasticity', manager: Andreas Frick,PhD.

The mammalian neocortex is central for sensory information processing, perception or control of motor activity, and cortical defects have devastating neurological and psychiatric consequences. One of the great contemporary challenges in neuroscience is the understanding of the function of neocortical circuits emerging from the integrative properties of the circuits’ neurons, their anatomical connectivity, and the physiological properties of these connections. A coordinated knowledge of these three dimensions will help us to understand the physiology of neuronal circuits and their pathology in CNS disorders.

During the last four years we have investigated various aspects of cortical circuit organization and their modulation during development, following activity patterns, or in disease. We have used a number of approaches, including electrophysiological, imaging, anatomical and behavioural methods. More recently, we have developed an improved viral approach to trace monosynaptically connected cells in vivo. Our major findings are as follows: 1) Cortical circuit organisation in the whisker-related barrel cortex changes during development in a cell identity-dependent manner. 2) Dendrites are important players for the overall information storage capacity of a neuron – dendritic plasticity is a mechanism for ‘metaplasticity’, and relies on signalling pathways different from those that induce synaptic plasticity. In addition, dendritic properties vary across the dendritic arbors of neocortical output neurons, setting up zones that possess specific signalling capabilities. Lastly 3) neocortex-dependent behavioural tasks demonstrate cognitive defects in Fmr1 knockout mice (mouse model for Fragile X Syndrome). In particular, results from a gap-crossing task suggest that Fmr1 knockout mice exhibit a hypersensitivity to sensory stimuli. This is in line with previous studies showing that Fragile X patients are hypersensitive to a range of sensory stimuli. Altogether, these findings provide new insight into the physiology and pathophysiology of cortical circuits and form the foundation of our future research project.


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