Cortical excitation and inhibition following focal traumatic brain injury.
Cortical excitation and inhibition following focal traumatic brain injury.
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DOI：
10.1523/jneurosci.3572-11.2011
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发表时间：
2011-10-05
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影响因子：
--
通讯作者：
Stanley GB
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文献类型：
--
作者：
Ding MC;Wang Q;Lo EH;Stanley GB
皮质受压在许多类型的脑损伤中可能是一个严重的问题，如脑创伤、局限性脑水肿、血肿、局灶性脑缺血或脑肿瘤。机械和细胞改变可导致神经元网络水平兴奋和抑制的全局变化，即使在没有组织学上显著的细胞损伤的情况下也是如此，通常表现为癫痫发作。然而，尽管这一问题的重要性和普遍性，脑损伤的确切电生理效应还没有得到很好的表征。在这项研究中，在感觉诱发的活体动物模型中，通过大规模、多电极测量初级躯体感觉皮质的多单位活动来表征持续皮质压迫后的电生理学变化。在远端损伤开始后，大鼠躯体感觉皮层的诱发反应立即出现一段时间的抑制，随后是高兴奋性，伴随着皮质激活的空间范围的增加。成对的脉冲触觉刺激显示兴奋/抑制动力学发生了戏剧性的变化，这表明在最初的抑制之后，大脑皮层环路出现了较长时间的过度兴奋，这可能与丘脑皮质环路的一个或多个抑制机制的破坏有关。总而言之，感觉诱发反应的使用为轻度损伤后果的演变提供了一个强大且可重复的功能标记物，是在体内量化创伤性脑损伤背景下皮质兴奋和抑制变化的重要一步。
Cortical compression can be a significant problem in many types of brain injuries, such as brain trauma, localized brain edema, hematoma, focal cerebral ischemia, or brain tumors. Mechanical and cellular alterations can result in global changes in excitation and inhibition on the neuronal network level even in the absence of histologically significant cell injury, often manifesting clinically as seizures. Despite the importance and prevalence of this problem, however, the precise electrophysiological effects of brain injury have not been well characterized. In this study, the changes in electrophysiology were characterized following sustained cortical compression using large-scale, multi-electrode measurement of multi-unit activity in primary somatosensory cortex in a sensory-evoked, in-vivo animal model. Immediately following the initiation of injury at a distal site, there was a period of suppression of the evoked response in the rat somatosensory cortex, followed by hyper-excitability that was accompanied by an increase in the spatial extent of cortical activation. Paired pulse tactile stimulation revealed a dramatic shift in the excitatory/inhibitory dynamics, suggesting a longer term hyperexcitability of the cortical circuit following the initial suppression that could be linked to the disruption of one or more inhibitory mechanisms of the thalamocortical circuit. Taken together, the use of a sensory-evoked response provided a robust and repeatable functional marker of the evolution of the consequences of mild injury, serving as an important step toward in vivo quantification of alterations in excitation and inhibition in the cortex in the setting of traumatic brain injury.