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Abstract #14763 Published in IGR 8-4
Establishment of animal model of chronic optic nerve injury and pathological changes thereof: Experiment with cats
Lu L-Q; Zhu A-H; Lou M-Q; Cai R-J; Dong Y; Lu Y-CZhonghua Yi Xue Za Zhi 2006; 86: 2177-2181
OBJECTIVE: To establish an animal model of chronic optic nerve injury which is suitable for experimental research. METHODS: Dil, a tracer, was injected through the bone windows into the brain of 48 cats so as to mark the retinal ganglion cells (RGCs). Two weeks later the 48 cats were randomly divided into 6 equal groups. The normal group did not receive any other treatment. Eight other cats underwent sham operation. Imitating the clinical pterional approach, a balloon was implanted into the place under the optic nerve and chiasm in the other 32 cats, then the volume of the balloons were increased by injecting contrast agent at different times to cause the optic nerve and chiasm compressed chronically for 1, 2, 4, or 6 weeks. Flash- visual evoked potential (F-VEP) was measured before operation and at the corresponding observation times in different groups. By the end of the experiment the cats were killed with the specimens of retina and optic nerve taken out to undergo light microscopy and electron microscopy to observe the pathological changes. Eight eyes were taken out from each group to calculate the number of RCGs 1, 2, 4, and 8 weeks after operation respectively. RESULTS: Microscopy showed that the retina showed profound morphological changes 8 weeks after compression; demyelination of optic nerve began to occur 2 weeks after compression and progressed later. Axonal degeneration was found 4 weeks after compression and became more significant 8 weeks later. Under electron microscopy, pathological changes of retina was found 4 weeks and more prominent 8 weeks after compression; slight demyelination and disorganized of cytoskeleton in the optic nerve were shown 2 weeks after compression, and became more profound later. Myelin regeneration was found 8 weeks after compression. The number of RGCs was reduced significantly by 37% (293/465) since 8 weeks after compression. F-VEP recording showed an extension of latency and depression of amplitude 4 weeks after compression, and the changes were more significant 8 weeks later. CONCLUSION: An animal model of chronic optic nerve injury by compression has been established which is stable and well repeatable. The pathological changes of compressed optic nerve are aggravated gradually as the compression lasts and the volume increases. Degeneration of RGCs occurs secondarily and obviously later than the axonal degeneration. LA: Chinese
Dr. Y.-C. Lu, Shanghai Institute of Neurosurgery, Department of Neurosurgery, Changzheng Hospital, Shanghai 200003, China
Classification:
5 Experimental glaucoma; animal models
2.15 Optic nerve (Part of: 2 Anatomical structures in glaucoma)
