MICE SPINAL CORD CM

Neuronal circuitry and plasticity of the spinal cord using in-vivo electrophysiology in transgenic mice

Coordinatore	KOBENHAVNS UNIVERSITET    more  Organization address postcode: 1017 contact info Titolo: Prof. Nome: Hans R Cognome: Hultborn Email: send email Telefono: -35327416 Fax: -35327454
Nazionalità Coordinatore	Denmark [DK]
Totale costo	0 €
EC contributo	203˙817 €
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-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2009
Periodo (anno-mese-giorno)	2009-12-01   -   2011-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	KOBENHAVNS UNIVERSITET	DK	coordinator	203˙817.53

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 Obiettivo del progetto (Objective)

'The development of transgenic mice affecting development of spinal cord circuitry or mimicking hereditary neurological motor disorders has necessitated the development of in-vivo adult mouse preparations for electrophysiology to bridge molecular biology with the pathophysiology of phenotypes. The first goal is the development and refinement of a “mouse in-vivo spinal cord preparation” for intracellular recordings and analysis of spinal circuitry in “acute experiments” and a preparation for chronic recording of EMG and kinematics. These will be used to identify specific patterns of inputs to motoneurones in the mouse including the Ia monosynaptic EPSP, presynaptic inhibition, reciprocal inhibition, recurrent inhibition, propioceptive and exteroceptive polysynaptic inputs as well as the intrinsic properties of motoneurones. The data will not only characterise synaptic connectively in the mouse which can be compared to other species but will serve as control data for the rest of the project. The second goal is the use of the preparations to study transgenic mice with specific manipulations affecting the development of spinal neuronal circuitry. 2 mice mutants developed by Thomas Jessell (New York) and Silvia Arber (Basel) will be used. In the Er81 mutant mouse lack of a transcription factor causes Ia propioceptive afferents to terminate prematurely in the intermediate spinal cord. The second mutant model lacks the presynaptic GABAergic terminals on Ia afferent inputs to motoneurones. The researcher will investigate the plasticity occurring as a consequence. The third goal is to use the preparations to study transgenic mice with genetic mutations similar to those underlying neurological disorders in humans. For this the researcher will investigate plasticity in mice with a mutation affecting the glycine receptor, mimicking hyperekplexia in humans. SOD-1 mutants, models of ALS will also be used to investigate excitability changes at central part of motoneurone'

Introduzione (Teaser)

The human central nervous system comprising of the brain and spinal cord is a complex system that is critical for normal functioning. Studying such a system is an even more complex endeavour.