| 摘要: |
| 目的:观察视神经慢性受压后视神经胶质细胞的病理改变,探讨胶质细胞与神经元的相互作用,为慢性视神经损伤的修复研究提供基础。方法:30只成年家猫随机等分为正常对照组、假手术组、压迫1周组、压迫2周组、压迫4周组和压迫8周组(n=5)。后4组利用球囊植入法建立慢性视神经损伤模型。各组动物灌注固定,取视神经组织,行透射电镜观察和免疫组织化学染色,观察胶质纤维酸性蛋白(GFAP)、髓磷脂碱性蛋白(MBP)、碳酸酐酶Ⅱ(CAⅡ)和ED-1的表达变化。结果:电镜下正常视神经髓鞘结构完整,各髓板清晰、排列紧密;受压2周后见轻微脱髓鞘;4周后出现板层分离、髓鞘泡状解离,并可见变性的胶质细胞;8周后髓鞘崩解更为明显,大部分髓鞘明显变薄,并可见凋亡小体形成。免疫组化染色在受压2周后无明显改变;4周后视神经MBP染色出现排列紊乱,有缺失现象;8周后染色缺失更为明显。受压4周后视神经压迫区出现CAⅡ染色紊乱,有缺失现象;8周后更为明显。非压迫区在受压8周后CAⅡ染色仍基本正常。受压4周后视神经直接受压区GFAP染色强度下降,损伤区近侧端染色强度增加;至8周时更为明显。正常视神经内可见散在的ED-1染色阳性细胞;受压4周后损伤区周围ED-1染色阳性细胞明显增多;8周后更为明显。结论:视神经慢性受压后损伤区出现胶质细胞变性和坏死,损伤区周围出现星形胶质细胞增殖和小胶质细胞激活,提示胶质细胞改变参与了慢性视神经损伤的病理过程。 |
| 关键词: 慢性视神经损伤 少突胶质细胞 星形胶质细胞 小胶质细胞 病理学 |
| DOI：10.3724/SP.J.1008.2009.0694 |
| 投稿时间：2008-11-22修订日期：2009-03-23 |
| 基金项目:国家自然科学基金(30271333),国家自然科学基金青年科学基金项目(30600635). |
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| Pathological changes of glial cells following chronic optic nerve compression |
| LV Li-quan,LOU Mei-qing,DONG Yan,CAI Ru-jue,HU Guo-han,LUO Chun,HOU Li-jun,LU Yi-cheng* |
| (Department of Neurosurgery,Shanghai Institute of Neurosurgery,Changzheng Hospital,Second Military Medical University,Shanghai 200003,China) |
| 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 anhydraseⅡ(CAⅡ ) 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 CAⅡ 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. |
| Key words: chronic optic nerve injuries oligodendrocyte astrocyte microglia pathology |
