Li Shihong, Kuroiwa Toshihiko, Ishibashi Satoru, Sun Liyuan, Endo Shu, Ohno Kikuo
Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.
Neurosci Lett. 2006 Dec 6;409(3):182-6. doi: 10.1016/j.neulet.2006.09.054. Epub 2006 Oct 9.
Mild traumatic brain injury (MTBI) may frequently cause transient behavioral abnormalities without observable morphological findings. In this study, we investigated neuropathological mechanisms underlying transient cognitive deficits after MTBI. Mongolian gerbils were subjected to experimental MTBI. At various time points after injury, behavioral changes were evaluated by the open-field test and T-maze test, and immunohistochemistry of microtubule-associated protein (MAP2) and amyloid precursor protein (APP) was performed to examine disruptions of the neuronal cytoskeleton and axonal transport, respectively. Transient cognitive deficits were observed after MTBI. Sustained MAP2 loss was found within the cortical impact site, but not the hippocampus. Transient APP accumulation at the same time as transient cognitive deficits occurred in the ipsilateral hemisphere, particularly in the subcortical white matter. These results suggest that the axonal dysfunction indicated by the reversible APP accumulation in the white matter, but not the sustained neuronal cytoskeletal damage reflected by the cortical MAP2 loss confined to the impact site, is responsible for the transient functional deficits after MTBI.
轻度创伤性脑损伤（MTBI）可能经常导致短暂的行为异常，而无明显的形态学改变。在本研究中，我们调查了MTBI后短暂认知缺陷的神经病理学机制。将蒙古沙鼠进行实验性MTBI。在损伤后的不同时间点，通过旷场试验和T迷宫试验评估行为变化，并分别进行微管相关蛋白（MAP2）和淀粉样前体蛋白（APP）的免疫组织化学检测，以检查神经元细胞骨架和轴突运输的破坏情况。MTBI后观察到短暂的认知缺陷。在皮质撞击部位发现MAP2持续丢失，但海马体未出现。在同侧半球，特别是在皮质下白质中，与短暂认知缺陷同时出现短暂的APP积聚。这些结果表明，白质中可逆的APP积聚所表明的轴突功能障碍，而非局限于撞击部位的皮质MAP2丢失所反映的持续性神经元细胞骨架损伤，是MTBI后短暂功能缺陷的原因。
