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Neural Regen Res. 2014 Mar 15;9(6):565-74. doi: 10.4103/1673-5374.130093.

Mechanisms of secondary degeneration after partial optic nerve transection.

Author information

1
Department of Ophthalmology, the University of Hong Kong, Hong Kong Special Administrative Region, China ; State Key Laboratory of Brain and Cognitive Science, the University of Hong Kong, Hong Kong Special Administrative Region, China.
2
GHM Institute of CNS Regeneration, Jinan University, Guangzhou, Guangdong Province, China ; Guangdong Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, Guangdong Province, China.
3
Department of Ophthalmology, the University of Hong Kong, Hong Kong Special Administrative Region, China ; GHM Institute of CNS Regeneration, Jinan University, Guangzhou, Guangdong Province, China ; Guangdong Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, Guangdong Province, China ; State Key Laboratory of Brain and Cognitive Science, the University of Hong Kong, Hong Kong Special Administrative Region, China.

Abstract

Secondary degeneration occurs commonly in the central nervous system after traumatic injuries and following acute and chronic diseases, including glaucoma. A constellation of mechanisms have been shown to be associated with secondary degeneration including apoptosis, necrosis, autophagy, oxidative stress, excitotoxicity, derangements in ionic homeostasis and calcium influx. Glial cells, such as microglia, astrocytes and oligodendrocytes, have also been demonstrated to take part in the process of secondary injury. Partial optic nerve transection is a useful model which was established about 13 years ago. The merit of this model compared with other optic nerve injury models used for glaucoma study, including complete optic nerve transection model and optic nerve crush model, is the possibility to separate primary degeneration from secondary degeneration in location. Therefore, it provides a good tool for the study of secondary degeneration. This review will focus on the research progress of the mechanisms of secondary degeneration using partial optic nerve transection model.

KEYWORDS:

astrocyte; calcium overload; excitotoxicity; macrophage; mitochondrion; oligodendrocyte; optic nerve; oxidative stress; partial injury; secondary degeneration

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