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Effect of long-term weightlessness on retina and optic nerve in tail-suspension rats

机译:长期失重对尾悬浮大鼠视网膜和视神经的影响

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摘要

AIM: To evaluate the effect of long-term weightlessness on retina and optic nerve in tail-suspension (TS) rats.METHODS: A stimulated weightlessness model was established by suspending rats’ tail. After 12wk, the ultrastructure and the number of optic nerve axons were observed by transmission electron microscope. The number of survival retinal ganglion cells (RGCs) was calculated by fluorescent gold retrograde labeling. Retina cells apoptosis was detected by TUNEL staining. The function of optic nerve and retina was evaluated by the visual evoked potential (VEP) and oscillatory potentials (Ops).RESULTS: The optic nerve axons were swollen and sparsely aligned, and the lamellar separation and myelin disintegration occurred after 12wk in TS rats. The density of optic nerve axons was 32.23±3.92 (vs 37.43±4.13, P=0.0145), the RGCs density was 1645±46 cells/mm2 (vs 1867±54 cells/mm2 P=0.0000), the incidence rate of retinal cells apoptosis was 5.38%±0.53% (vs 4.75%±0.54%, P=0.0238), the amplitude of VEP-P100 was 15.43±2.14 µV (vs 17.67±2.17 µV, P=0.0424), the latency of VEP-P100 was 69.05±5.34ms (vs 62.43±4.87ms P=0.0143) and the sum amplitude of Ops was 81.05±8.34 µV (vs 91.67±10.21 µV, P=0.0280) in TS group and the control group, respectively.CONCLUSION: Long-term weightlessness can induce the ultrastructural changes and functional depress of the optic nerve, as well as retinal cell damages in TS rats.
机译:目的:评价长期无重量对尾悬浮(TS)大鼠视网膜和视神经的影响。方法:通过悬挂大鼠尾部建立刺激的失重模型。在12wk之后,通过透射电子显微镜观察超微结构和视神经轴突的数量。通过荧光金逆行标记计算存活视网膜神经节细胞(RGC)的数量。 Turine染色检测到视网膜细胞凋亡。视神经和视网膜的功能通过视觉诱发电位(VEP)和振荡电位(OPS)评估。结果:视神经轴突溶胀并稀疏对齐,并在TS大鼠12wk后发生层状分离和髓鞘崩解。视神经轴承的密度为32.23±3.92(Vs 37.43±4.13,P = 0.0145),RGCS密度为1645±46个细胞/ mm2(与1867±54个细胞/ mm2 p = 0.0000),视网膜细胞发生率细胞凋亡为5.38%±0.53%(Vs 4.75%±0.54%,p = 0.0238),Vep-p100的幅度为15.43±2.14μV(Vs 17.67±2.17μV,p = 0.0424),Vep-P100的潜伏期是69.05±5.34ms(Vs 62.43±4.87ms P = 0.0143)分别在TS组和对照组中,OPS的总和幅度为81.05±8.34μV(Vs 91.67±10.21μV,p = 0.0280)。结论:长期失重可以诱导视神经的超微结构变化和功能压力,以及TS大鼠的视网膜细胞损伤。

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