Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/72461
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Type: Journal article
Title: The mechanism of axonal degeneration after perikaryal excitotoxic injury to the retina
Author: Bull, N.
Chidlow, G.
Wood, J.
Martin, K.
Casson, R.
Citation: Experimental Neurology, 2012; 236(1):34-45
Publisher: Academic Press Inc Elsevier Science
Issue Date: 2012
ISSN: 0014-4886
1090-2430
Statement of
Responsibility: 
Natalie D. Bull, Glyn Chidlow, John P.M. Wood, Keith R. Martin, Robert J. Casson
Abstract: We investigated the mechanism of secondary axonal degeneration after perikaryal excitotoxic injury to retinal ganglion cells (RGCs) by comparing pathological responses in wild-type rats and Wld(s) rats, which display delayed Wallerian degeneration. After perikaryal excitotoxic RGC injury, both types of rats exhibited a spatio-temporal pattern of axonal cytoskeletal degeneration consistent with Wallerian degeneration, which was delayed by up to 4 weeks in Wld(s) rats. Furthermore, RGC somal loss was greater in Wld(s) rats. Microglial response in the anterior visual pathway to injury was attenuated in the Wld(s) rats with lymphocytic infiltration that was relatively reduced; however, immunostaining for major histocompatibility complex class II antigens (OX6) was more pronounced in Wld(s) rats. These data indicate that perikaryal excitotoxic RGC injury causes a secondary Wallerian axonal degeneration, and support the notion of a labile, soma-derived axonal survival factor.
Keywords: Excitotoxicity; Wallerian; Neurodegeneration
Rights: Copyright © 2012 Elsevier Inc. All rights reserved.
RMID: 0020119404
DOI: 10.1016/j.expneurol.2012.03.021
Appears in Collections:Opthalmology & Visual Sciences publications

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