Myelination of axons is an essential step to ensure the rapid propagation of action potentials by saltatory conduction, a mechanism that relies on the nodes of Ranvier. These short unmyelinated axonal domains are highly enriched in voltage-gated sodium channels (Nav), which allow the regeneration and propagation of the action potentials by depolarization of the plasma membrane. Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS), which corresponds to the first source of non-traumatic neurological handicap in young adults in Europe and the USA. It is a complex disease with an inflammatory process associated to demyelinating attacks, followed by repair of the lesioned brain and spinal cord. The repair process (remyelination), relying on precursor cells of the oligodendrocytes (the myelinating glial cells of the CNS) can be extensive, but remains most of the time insufficient, leading to irreversible damages of the denuded axons associated with permanent neurological deficits. Treatments available presently only target the immune aspect of MS, and although they allow to decrease the frequency of relapses, their efficiency on long term progression of the disease is not proven. Promoting repair in order to protect axons and limit handicap progression is thus one of the key challenges in MS.
Our research group focuses on the mechanisms underlying (re)myelination in the central nervous system. We are in particular interested in how to promote an adequate repair following demyelination, using various models ranging from in vitro primary cell cultures to demyelinating models in mouse.
In the present project, supported by an ANR Jeunes Chercheurs, we want to focus on the mechanisms of early node of Ranvier reassembly following demyelination and how it could participate in the dialog between demyelinated neurons and the various surrounding glial cell types participating in the remyelination process. In particular, we want to evaluate whether these interactions could have an impact on remyelination modulation and neuroprotection.
Applicants should have completed a PhD in Neurosciences (see detailed profile below) and have less than 1 year post-doctoral experience.
Full applications including curriculum vitae, list of publications and 2 references should be sent to Dr Anne Desmazieres, Lubetzki-Stankoff team, ICM, Paris by e-mail : email@example.com.
You will be responsible of designing study protocols and perform experiments related to the ANR JC project
You will collaborate with other members of the research group, as well as external collaborators.
You will be responsible of overseeing the cultures and animals used and of reporting and participating in the publication of the obtained results
You have a PhD in neurobiology / neuroscience related to myelination, multiple sclerosis models, neuronal activity or developmental fields
You have an expertise in cell or slice cultures and/or in vivo studies in mouse models (surgery skills appreciated)
You have an expertise in imaging, in particular live-imaging (videomicroscopy, spinning disk or 2 photon imaging, calcium-imaging…) and/or optogenetics
An experience in DREADD’s technique and/or use of various drugs and (ant)agonists to study signaling pathways in the central nervous system would be appreciated
We offer you a post-doc position for one year and a half, with a potential opportunity for renewal. You will also be supported to apply for a personal postdoctoral fellowship.
If interested, please contact Dr Anne Desmazieres, e-mail: firstname.lastname@example.org; phone number : +33(0)1 57 27 44 63