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首页> 外文期刊>The European Journal of Neuroscience >Differential changes in axonal conduction following CNS demyelination in two mouse models.
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Differential changes in axonal conduction following CNS demyelination in two mouse models.

机译：在两个小鼠模型中，中枢神经系统脱髓鞘后，轴突传导的差异性变化。

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Transgenic and disease model mice have been used to investigate the molecular mechanisms of demyelinating diseases. However, less attention has been given to elucidating changes in nerve conduction in these mice. We established an experimental system to measure the response latency of cortical neurons and examined changes in nerve conduction in cuprizone-induced demyelinating mice and in myelin basic protein-deficient shiverer mice. Stimulating and recording electrodes were placed in the right and left sensori-motor cortices, respectively. Electrical stimulation of the right cortex evoked antidromic responses in left cortical neurons with a latency of 9.38 +/- 0.31 ms (n = 107; mean +/- SEM). While response latency was longer in mice at 7 days and 4 weeks of cuprizone treatment (12.35 +/- 0.35 ms, n = 102; 11.72 +/- 0.29 ms, n = 103, respectively), response latency at 7 days and 4 weeks after removal of cuprizone was partially restored (10.72 +/- 0.45 ms, n = 106; 10.27 +/- 0.34 ms, n = 107, respectively). Likewise, electron microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone removal. We also examined whether the myelin abnormalities in shiverer mice affected their response latencies. But there were no significant differences in response latencies in shiverer (9.83 +/- 0.24 ms, n = 103) and wild-type (9.33 +/- 0.22 ms, n = 112) mice. The results of these electrophysiological assessments imply that different demyelinating mechanisms, differentially affecting axon conduction, are present in the cuprizone-treated and shiverer mice, and may provide new insights to understanding the pathophysiology of demyelination in animal models in the CNS.
机译：转基因和疾病模型小鼠已用于研究脱髓鞘疾病的分子机制。但是，很少有人关注阐明这些小鼠神经传导的变化。我们建立了一个实验系统来测量皮质神经元的反应潜伏期，并检查了铜酮诱导的脱髓鞘小鼠和髓鞘碱性蛋白缺乏的颤抖小鼠中神经传导的变化。刺激和记录电极分别放置在右和左感觉运动皮层中。右皮质的电刺激在左皮质神经元中引起抗体反应，潜伏期为9.38 +/- 0.31 ms（n = 107;平均值+/- SEM）。铜酮治疗7天和4周时小鼠的反应潜伏期较长（分别为12.35 +/- 0.35毫秒，n = 102; 11.72 +/- 0.29 ms，n = 103），但反应潜伏期在7天和4周时去除铜酮后部分恢复（分别为10.72 +/- 0.45毫秒，n = 106; 10.27 +/- 0.34毫秒，n = 107）。同样，电子显微镜检查显示铜cup诱导的call体脱髓鞘作用，去除铜riz后几乎完全重新髓鞘化。我们还检查了颤抖小鼠的髓磷脂异常是否影响其反应潜伏期。但是，颤抖（9.83 +/- 0.24 ms，n = 103）和野生型（9.33 +/- 0.22 ms，n = 112）小鼠的反应潜伏期没有显着差异。这些电生理学评估的结果表明，在铜酮治疗和颤抖的小鼠中存在不同的脱髓鞘机制，差异地影响轴突传导，并且可能为了解CNS动物模型中脱髓鞘的病理生理学提供新的见解。

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