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Research fields
Team 04:
Physiology and therapeutic
approaches of spinal cord pathologies
Head: Alain Privat, DR1
Traumatic lesions of the
spinal cord constitute a privileged model for the development
of repair strategies for the central nervous system.
Neuroprotection studies follow two directions:
Upstream, we concentrate upon a series of molecules
which are high-affinity non-competitive antagonists
of the NMDA receptor. We are currently analyzing with
molecular probes the precise targets of these molecules.
Downstream, we have developed a technology of high resolution
MRI applied to mouse models to decipher in real time
the early events of spinal cord injury. Finally, functional
consequences of the lesion are analyzed with automated
analysis of locomotion.
Contact : hirbec@montp.inserm.fr |
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Axonal regeneration is a key issue following a CNS
lesion. We concentrate our efforts in this area on the control
of the formation of obstructive glial scar. We have already
brought a proof of principle of the importance of the astrocytic
scar thanks to the use of Mice KO for the main astrocytic
cytoskeletal proteins, GFAP and Vimentin. We are now translating
this approach for therapeutic purposes with siRNA
directed against the synthesis of these proteins.
Contact : privat@univ-montp2.fr
Neural stem cells. These
cells persist in the adult spinal cord near the central
canal. In vitro, they differentiate into neurons and glial
cells. We seek to understand the molecular mechanisms of
self-renewal/differentiation, and the molecular interactions
neural stem cells make in the ependymal niche. Besides,
we have demonstrated that sublesional transplants of monoaminergic
neurons can activate the Central Pattern Generator of locomotion
(CPG), and urogenital sphere. We are currently elaborating
therapeutic strategies based on the graft of genetically
transformed non neural cells, and of stem cells to produce
monoaminergic neurons.
Contact : hugnot@univ-montp2.fr
In the area of neurodegenerative diseases,
the concentrated area effort on Kennedy disease, or SBMA,
which is characterized by the presence of plyglutamine sequences
in the androgen receptor, which lend to the destruction of
motoneurones. We have elaborated an in-vitro model of the
disease on which we are probing various physiopathological
hypotheses and corresponding therapeutic strategies.
Contact : norbert.bakalara@enscm.fr
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