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Electrophysiological monitoring of injury progression in the rat cerebellar cortex

机译:大鼠小脑皮层损伤进程的电生理监测

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摘要

The changes of excitability in affected neural networks can be used as a marker to study the temporal course of traumatic brain injury (TBI). The cerebellum is an ideal platform to study brain injury mechanisms at the network level using the electrophysiological methods. Within its crystalline morphology, the cerebellar cortex contains highly organized topographical subunits that are defined by two main inputs, the climbing (CFs) and mossy fibers (MFs). Here we demonstrate the use of cerebellar evoked potentials (EPs) mediated through these afferent systems for monitoring the injury progression in a rat model of fluid percussion injury (FPI). A mechanical tap on the dorsal hand was used as a stimulus, and EPs were recorded from the paramedian lobule (PML) of the posterior cerebellum via multi-electrode arrays (MEAs). Post-injury evoked response amplitudes (EPAs) were analyzed on a daily basis for 1 week and compared with pre-injury values. We found a trend of consistently decreasing EPAs in all nine animals, losing as much as 72 ± 4% of baseline amplitudes measured before the injury. Notably, our results highlighted two particular time windows; the first 24 h of injury in the acute period and day-3 to day-7 in the delayed period where the largest drops (~50% and 24%) were observed in the EPAs. In addition, cross-correlations of spontaneous signals between electrode pairs declined (from 0.47 ± 0.1 to 0.35 ± 0.04, p < 0.001) along with the EPAs throughout the week of injury. In support of the electrophysiological findings, immunohistochemical analysis at day-7 post-injury showed detectable Purkinje cell loss at low FPI pressures and more with the largest pressures used. Our results suggest that sensory evoked potentials (SEPs) recorded from the cerebellar surface can be a useful technique to monitor the course of cerebellar injury and identify the phases of injury progression even at mild levels.
机译:受影响的神经网络中兴奋性的变化可以用作研究创伤性脑损伤(TBI)的时间过程的标记。小脑是使用电生理方法在网络水平研究脑损伤机制的理想平台。在其晶体形态内,小脑皮质包含高度组织的地形亚基,由两个主要输入(攀爬(CFs)和苔藓纤维(MFs))定义。在这里,我们证明了通过这些传入系统介导的小脑诱发电位(EPs)的使用,以监测液体敲打损伤(FPI)大鼠模型中的损伤进展。使用背侧手的机械敲打作为刺激,并通过多电极阵列(MEA)从小脑后的旁中叶(PML)记录EP。每天分析损伤后诱发的反应幅度(EPA)1周,并与损伤前的值进行比较。我们发现所有九只动物的EPA持续下降的趋势,导致受伤前测量的基线幅度下降多达72±4%。值得注意的是,我们的结果突出了两个特定的时间窗口;在急性期的第一个24小时内,在延误期的第3天到第7天,在EPA中观察到最大的跌落(〜50%和24%)。此外,在整个损伤周中,电极对之间的自发信号的互相关性从EPA下降了(从0.47±0.1到0.35±0.04,p <0.001)。为了支持电生理学结果,损伤后第7天的免疫组织化学分析显示,在低FPI压力下以及在使用最大压力的情况下,可检测到的Purkinje细胞丢失。我们的研究结果表明,从小脑表面记录的感觉诱发电位(SEP)可能是一种有用的技术,可监测小脑损伤的过程并确定损伤进展的阶段,即使在轻度水平下也是如此。

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