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Tellurium‐induced demyelination: An electrophysiological and morphological study

机译:碲诱导的脱髓鞘:电生理学和形态学研究

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AbstractTellurium (Te) is a naturally occurring element with many industrial uses. Microinjection of 0.3 μg of potassium tellurite K(2)TeO(3) into the endoneurial space of rat tibial nerve causes a rapidly progressing focal conduction block as measured by the disappearance of the evoked compound muscle action potential (CAMP) of the intrinsic foot muscles following stimulation proximal to the injection site. Conduction block was fully established within 6 hours and persisted for approximately 7 days, followed by the appearance of low amplitude, long latency, temporally dispersed potentials. The proximal CMAPs increased in amplitude and decreased in latency and temporal dispersion until normalization by 28 days after injection. The distal CMAP showed a minimal decline in amplitude. Morphological observations showed splitting of myelin, especially in the paranodal regions, followed by accumulation of myelin debris in Schwann cells and macrophages. Although the exact mechanism remains unknown, this in vivo model provides a unique opportunity to study the electrophysiological and morphological correlates of an acutely evolving demyelinative process
机译:摘要 碲(Te)是一种天然存在的元素,具有许多工业用途。将 0.3 μg 碲酸钾 [K(2)TeO(3)] 显微注射到大鼠胫神经的神经内腔中会导致快速进展的局灶性传导阻滞,这可以通过注射部位近端刺激后内足肌肉的诱发复合肌肉动作电位 (CAMP) 的消失来测量。传导阻滞在 6 小时内完全建立并持续约 7 天,随后出现低振幅、长潜伏期、时间分散电位。近端CMAP的振幅增加,潜伏期和时间分散度降低,直到注射后28天恢复正常。远端CMAP的振幅下降幅度最小。形态学观察显示髓鞘分裂,特别是在副结区域,随后髓鞘碎片在雪旺细胞和巨噬细胞中积累。尽管确切的机制仍然未知,但这种体内模型为研究急性进化的脱髓鞘过程的电生理学和形态学相关性提供了一个独特的机会

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