Bhowmick Saurav, D'Mello Veera, Ponery Nizmi, Muneer P M Abdul
Laboratory of CNS Injury and Repair, Neuroscience Institute, JFK Medical Center, 65 James St, Edison, NJ 08820, USA.
Brain Sci. 2018 Jan 6;8(1):11. doi: 10.3390/brainsci8010011.
Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits, which occur through a cascade of deleterious pathophysiological events over time. In this study, we investigated the hypothesis that neurodegeneration caused by TBI leads to impairments in sensorimotor function. TBI induces the activation of the caspase-3 enzyme, which triggers cell apoptosis in an in vivo model of fluid percussion injury (FPI). We analyzed caspase-3 mediated apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and poly (ADP-ribose) polymerase (PARP) and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, the inverted screen test, and the climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.
创伤性脑损伤（TBI）可导致持续的感觉运动和认知缺陷，这些缺陷会随着时间的推移通过一系列有害的病理生理事件而出现。在本研究中，我们调查了TBI引起的神经退行性变导致感觉运动功能受损的假说。TBI诱导半胱天冬酶-3酶的激活，该酶在液体冲击伤（FPI）的体内模型中触发细胞凋亡。我们通过末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色、聚（ADP-核糖）聚合酶（PARP）和膜联蛋白V免疫印迹分析半胱天冬酶-3介导的细胞凋亡。我们通过进行包括网格行走、平衡木、倒屏试验和攀爬试验在内的动物行为测试，将神经退行性变与感觉运动缺陷相关联。我们的研究表明，过度的细胞死亡或神经退行性变与TBI相关的神经元功能障碍和感觉运动损伤有关。
