An in vitro model to study inhibition of sensory and motor axon regeneration mediated by Guillain Barrè Syndrome-associated anti-glycan antibodies.

VICTORIA ROZÉS SALVADOR, ANABELA PALANDRI, PABLO H. H. LÓPEZ

Huerta Grande, Còrdoba

Congreso; Congreso de la Sociedad Argentina de Neurociencias; 2011

Sociedad Argentina de Neurociencias

  Axon regeneration is a response of injured nerve cells that is critical for the restoration of structure and function after PNS or CNS injuries; this response is key to recover from numerous neurological disorders like acute immune neuropathy called Guillain Barré Syndrome (GBS). Some clinical studies associate the presence of anti- ganglioside antibodies (anti-Gg abs) with poor recovery in GBS. Patients with incomplete recovery have failure of nerve repair. We recently demonstrated in a passive transfer animal model that anti-Gg abs can halt axon regeneration. Defining the signaling pathways that prevent regeneration of injured axons can provide key insights to allow development of therapeutic approaches to enhance axon growth. For this reason, we developed an in vitro model of axon regeneration using organotypic co-cultures of spinal cord or dorsal root ganglion explants with peripheral nerve. Inhibition was produced by treating cultures with an anti-Gg mAb (GD1a/GT1b). Also, cultures were infected with VSV-G-pseudotyped lentivirus vector carrying the GFP sequence taking advantage of its greater trofism for neurons to keep track of regenerating axons on nerves. This model will be a useful tool to study the effect of anti-Gg Abs on the cytoskeleton of dystrophic growth cones.