Transneuronal Degeneration of Thalamic Nuclei following Middle Cerebral Artery Occlusion in Rats.
Transneuronal Degeneration of Thalamic Nuclei following Middle Cerebral Artery Occlusion in Rats.
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DOI：
10.1155/2016/3819052
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发表时间：
2016
影响因子：
--
通讯作者：
Hsu ML
中科院分区：
文献类型：
--
作者：
Chang SJ;Cherng JH;Wang DH;Yu SP;Liou NH;Hsu ML
客观的。梗死后跨神经元变性是指在持续缺血性损伤的突触神经元的输入或输出中断后几天至几周内发生的继发性神经元死亡。丘脑从后循环获得血液供应；然而，大脑中动脉梗塞可能导致丘脑继发性跨神经元变性。在这项研究中，我们展示了大鼠模型中 MCAo 后的缺血区域和相关的跨神经元变性。材料和方法。 18 只 12 周龄雄性 Sprague-Dawley 大鼠被随机分配接受大脑中动脉阻塞手术 1、7 和 14 天。通过2,3,5-三苯基四唑盐酸盐染色评估脑萎缩。在处死动物之前进行姿势反射和旷场测试，以评估闭塞对行为的影响。结果。缺血后在病变部位观察到髓鞘质损失。闭塞后 14 天，丘脑区域也观察到神经胶质增生。在梗塞的各个阶段观察到血管内皮生长因子表达增加的不同程度。在 14 天组中还观察到髓磷脂碱性蛋白水平增加。结论。目前的大鼠缺血模型提供了闭塞前 14 天内跨神经元变性的证据。观察到的蛋白质表达变化可能与受损大脑的自我修复机制有关。
Objective. Postinfarction transneuronal degeneration refers to secondary neuronal death that occurs within a few days to weeks following the disruption of input or output to synapsed neurons sustaining ischemic insults. The thalamus receives its blood supply from the posterior circulation; however, infarctions of the middle cerebral arterial may cause secondary transneuronal degeneration in the thalamus. In this study, we presented the areas of ischemia and associated transneuronal degeneration following MCAo in a rat model. Materials and Methods. Eighteen 12-week-old male Sprague-Dawley rats were randomly assigned to receive middle cerebral artery occlusion surgery for 1, 7, and 14 days. Cerebral atrophy was assessed by 2,3,5-triphenyltetrazolium hydrochloride staining. Postural reflex and open field tests were performed prior to animal sacrifice to assess the effects of occlusion on behavior. Results. Myelin loss was observed at the lesion site following ischemia. Gliosis was also observed in thalamic regions 14 days following occlusion. Differential degrees of increased vascular endothelial growth factor expression were observed at each stage of infarction. Increases in myelin basic protein levels were also observed in the 14-day group. Conclusion. The present rat model of ischemia provides evidence of transneuronal degeneration within the first 14 days of occlusion. The observed changes in protein expression may be associated with self-repair mechanisms in the damaged brain.