NEURO-GLIAL SYNAPSES

Neuronal Activity: Targets for Stimulating Myelin Formation and Repair in the Brain

Coordinatore	THE UNIVERSITY OF BIRMINGHAM    more  Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT contact info Titolo: Ms. Nome: May Cognome: Chung Email: send email Telefono: 441214000000 Fax: 441214000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	72˙916 €
EC contributo	72˙916 €
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-2011-CIG
Funding Scheme	MC-CIG
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-09-01   -   2014-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE UNIVERSITY OF BIRMINGHAM  Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT contact info Titolo: Ms. Nome: May Cognome: Chung Email: send email Telefono: 441214000000 Fax: 441214000000	UK (BIRMINGHAM)	coordinator	27˙083.34
2	THE UNIVERSITY OF WARWICK  Organization address address: Kirby Corner Road - University House - city: COVENTRY postcode: CV4 8UW contact info Titolo: Dr. Nome: Peter Cognome: Hedges Email: send email Telefono: +44 247 652 3716 Fax: +44 247 652 4991	UK (COVENTRY)	participant	45˙833.33

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 Obiettivo del progetto (Objective)

'Neurological disorders associated with dysfunctional and damaged myelin represent a heavy economic and social burden within the EU. Therefore identifying novel targets for stimulating myelin formation and repair hold significant value. Neuronal activity influences the development of myelinating glia and the formation of myelin in the brain. However the physiological basis of these neuron-glial interactions are poorly described in the context of intact nervous tissues. This work will focus on receptors that are capable of integrating neuronal activity with oligodendrocyte function. Neuronal activity stimulates ionotropic glutamate receptors located on oligodendrocyte precursor cells (OPCs). However the function of these neuron-OPC synapses in the nervous system is unknown. Activation of these receptors regulates the migration and differentiation of oligodendrocyte precursor cells in vitro. By relaying information regarding axonal function these receptors are well positioned to translate changes in activity arising during development, and as a consequence of injury and disease, into signals capable of promoting the developmental programme required for myelination. Consequently these receptors represent valuable targets for stimulating neural repair in conditions of myelin disease and injury. These ideas will be tested by selectively disrupting glutamate receptor functions in OPCs with a series of novel genetically encoded tools. These tools will be deployed in slice cultures that permit the analysis of myelin formation and repair. The effect of these receptor manipulations will then be examined on axon-OPC interactions, OPC development, myelin formation, and myelin replacement. Illuminating mechanisms connecting axonal activity to myelin formation and recovery promises to stimulate novel therapies for myelin-associated disorders such as those underlying cerebral palsy in infants, and multiple sclerosis, which afflicts an estimated 405 thousand adults in the EU.'