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Title: Neurites regrowth of cortical neurons by GSK3b inhibition independently of Nogo Receptor 1
Author: Seira Oriach, Oscar
Gavín Marín, Rosalina
Gil, V.
Llorens Torres, Franc
Rangel, A.
Soriano García, Eduardo
Río Fernández, José Antonio del
Keywords: Neurones
Regeneració del sistema nerviós
Nervous system regeneration
Issue Date: 2010
Publisher: Wiley
Abstract: Lesioned axons do not regenerate in the adult mammalian central nervous system, owing to the overexpression of inhibitory molecules such as myelin-derived proteins or chondroitin sulphate proteoglycans. In order to overcome axon inhibition, strategies based on extrinsic and intrinsic treatments have been developed. For myelin-associated inhibition, blockage with NEP1-40, receptor bodies or IN-1 antibodies has been used. In addition, endogenous blockage of cell signalling mechanisms induced by myelin-associated proteins is a potential tool for overcoming axon inhibitory signals. We examined the participation of glycogen synthase kinase 3 (GSK3) and ERK1/2 in axon regeneration failure in lesioned cortical neurons. We also investigated whether pharmacological blockage of GSK3 and ERK1/2 activities facilitates regeneration after myelin-directed inhibition in two models: i) cerebellar granule cells and ii) lesioned entorhino-hippocampal pathway in slice cultures, and whether the regenerative effects are mediated by Nogo Receptor 1 (NgR1). We demonstrate that, in contrast to ERK1/2 inhibition, the pharmacological treatment of GSK3 inhibition strongly facilitated regrowth of cerebellar granule neurons over myelin independently of NgR1. Lastly these regenerative effects were corroborated in the lesioned EHP in NgR1 -/- mutant mice. These results provide new findings for the development of new assays and strategies to enhance axon regeneration in injured cortical connections.
Note: Versió preprint del document publicat a:
It is part of: Journal of Neurochemistry, 2010, vol. 113, num. 6, p. 1644-1658
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ISSN: 0022-3042
Appears in Collections:Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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