Academic Journal

Neurites regrowth of cortical neurons by GSK3β inhibition independently of Nogo Receptor 1

التفاصيل البيبلوغرافية
العنوان: Neurites regrowth of cortical neurons by GSK3β inhibition independently of Nogo Receptor 1
المؤلفون: Seira, Oscar, Gavin, Rosalina, Gil, Vanessa, Llorens, Franc, Rangel, Alejandra (R17729), Soriano, Eduardo, Rio, Jose A. del
بيانات النشر: U.K., Wiley-Blackwell
سنة النشر: 2010
المجموعة: University of Western Sydney (UWS): Research Direct
مصطلحات موضوعية: 060802 - Animal Cell and Molecular Biology, mammals, neurons, axons
الوصف: Lesioned axons do not regenerate in the adult mammalian CNS, owing to the over-expression 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 3β (GSK3β) and extracellular-related kinase (ERK) 1/2 in axon regeneration failure in lesioned cortical neurons. We also investigated whether pharmacological blockage of GSK3β and ERK1/2 activities facilitates regeneration after myelin-directed inhibition in two models: (i) cerebellar granule cells and (ii) lesioned entorhinohippocampal 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 GSK3β inhibition strongly facilitated regrowth of cerebellar granule neurons over myelin independently of NgR1. Finally, these regenerative effects were corroborated in the lesioned entorhino-hippocampal pathway 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.
نوع الوثيقة: article in journal/newspaper
وصف الملف: print
اللغة: English
Relation: Journal of Neurochemistry--0022-3042--1471-4159 Vol. 113 Issue. 6 pp: 1644-1658
DOI: 10.1111/j.1471-4159.2010.06726.x
الاتاحة: http://handle.uws.edu.au:8081/1959.7/uws:32395
https://doi.org/10.1111/j.1471-4159.2010.06726.x
رقم الانضمام: edsbas.243F19AF
قاعدة البيانات: BASE
الوصف
DOI:10.1111/j.1471-4159.2010.06726.x