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Academic Journal of Second Military Medical University ; (12): 694-698, 2010.
Article in Chinese | WPRIM | ID: wpr-840566

ABSTRACT

Objective: To examine the pathologcial changes of glial cells after chronic optic nerve compression, so as to discuss the interaction between the glial cells and neurons. Methods: Thirty adult cats were randomly divided into 6 groups (n= 5), namely, control group, sham operation group, 1-week compression group, 2-week compression group, 4-week compression group, and 8-week compression group. The chronic optic nerve injury model was produced by an inflatable balloon implanted under the optic chiasm in the latter 4 groups. All the animals were sacrificed and perfused; the optic nerves were removed and the cellular responses of the nerves were observed by electronic microscopy; and the expression of glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), carbonic anhydrase II (CA II) and ED-1 was exmined at various time points by immunohistochemical staining. Results: Under the electron microscopy, the normal optic nerves had integrated myelin structure, clearly and closely arranged neural plate. The optic nerve presented slight demyelination 2 weeks after compression; myelin laminalle dissociating and glial cell degenerating occurred 4 weeks after compression; and the demyelination became more obvious and the most myelin became thiner 8 weeks after compression. No obvious immunohistochemistral changes were found in the optic nerves during the first two weeks of compression. The MBP staining was disturbed and lost at 4 weeks after compression, which became more obvious 8 weeks after compression. The CA II staining in the compressed region was irregular and lost at 4 weeks, which was more obvious at 8 weeks; the staining in non-compressed region was normal. The intensity of GFAP staining was reduced in the compressed region and increased at proximal portion of the nerve at 4 weeks, which became more significant at 8 weeks. The ED-1 positive cells were found in the normal nerve with low density. The positive cells increased around the compressed region at 4 weeks and became more significant at 8 weeks. Conclusion: Glial cell degeneration and death occur in the compressive region afte chronic compression of optic nerve. The proximal portion of the compressed nerve has astrocyte proliferation and microglia activation, indicating that functional change of glial cells may contribute to chronic optic nerve injury.

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