Abstract：
Traumatic brain injury (TBI) is the leading cause of accident-related death and disability in the world and can lead to long-term neuropsychiatric symptoms, such as a decline in cognitive function and neurodegeneration. TBI includes primary and secondary injury, with head trauma and deformation of the brain caused by the physical force of the impact as primary injury, and cellular and molecular cascades that lead to cell death as secondary injury. Currently, there is no treatment for TBI-induced cell damage and neural circuit dysfunction in the brain, and thus, it is important to understand the underlying cellular mechanisms that lead to cell damage. In the current study, we use stretchable microelectrode arrays (sMEAs) to model the primary injury of TBI to study the electrophysiological effects of physically injuring cortical cells. We recorded electrophysiological activity before injury and then stretched the flexible membrane of the sMEAs to injure the cells to varying degrees. At 1, 24, and 72 h post-stretch, we recorded activity to analyze differences in spike rate, Fano factor, burstlet rate, burstlet width, synchrony of firing, local network efficiency, and Q statistic. Our results demonstrate that mechanical injury changes the firing properties of cortical neuron networks in culture in a time- and severity-dependent manner. Our results suggest that changes to electrophysiological properties after stretch are dependent on the strength of synchronization between neurons prior to injury.
摘要：
创伤性脑损伤（TBI）是世界上与事故相关的死亡和残疾的主要原因，并可导致长期的神经精神症状，如认知功能下降和神经变性。TBI包括原发性和继发性损伤，以撞击的物理力引起的头部创伤和大脑变形为主要伤害，以及导致细胞死亡的细胞和分子级联反应作为继发性损伤。目前,没有治疗TBI诱导的细胞损伤和大脑中的神经回路功能障碍，因此，了解导致细胞损伤的潜在细胞机制很重要。在目前的研究中,我们使用可拉伸微电极阵列（sMEAs）对TBI的原发性损伤进行建模，以研究物理损伤皮质细胞的电生理效应。我们记录了损伤前的电生理活动，然后拉伸sMEAs的柔性膜以不同程度地损伤细胞。拉伸后1、24和72小时，我们记录了活性以分析刺速的差异，法诺因素,突发率,Burstlet宽度,射击的同步性，本地网络效率，和Q统计。我们的结果表明，机械损伤以时间和严重程度相关的方式改变了培养中皮层神经元网络的放电特性。我们的结果表明，拉伸后电生理特性的变化取决于损伤前神经元之间的同步强度。
