Immunohistochemical and Ultrastructual Study of Brain Injury Produced by Repeated Impacts.

为探讨反复轻微撞击对脑组织病理生物学的影响，设计了2种实验性颅脑损伤模型。在活体内，成年大鼠使用由黄铜重量(450g)通过亚克力导管(1M)坠落组成的减重装置进行损伤。3次侮辱后，间隔24小时，用4%多聚甲醛在磷酸盐缓冲液中灌流并取出。组织病理学和免疫组织化学研究显示大脑皮层有神经元损伤，胼胝体有脑水肿。尽管缺乏弥漫性轴突改变，该模型将适合于研究与轻微头部创伤相关的神经元改变。用培养的细胞建立体外轴突损伤模型，通过相差显微镜和透射电子显微镜观察，介绍损伤对神经元突起的影响，并确定局部肿胀的形成机制。培养皿振荡…更多的一维和水平1、2或3次；每隔一小时重复一次，每次5秒；在加热控制的摇床上。振荡的幅度和频率分别为40 mm和1 Hz。损伤的突起有两种形式：突起末端直径增大和损伤部位珠状突起。显微镜下的发现表明，压力会破坏细胞骨架网络，然后导致细胞过程的球状变形。超微结构显示，小球含有紧密稀疏排列错位的细胞骨架，并显著聚集致密的囊泡。再生的生长锥体内的细胞骨架重建也在末端肿胀和珠子中被注意到。这些连接子的破坏将负责启动细胞骨架的破坏。然而，细胞骨架改变的起始点必须通过不含可溶性蛋白的样品的三维成像和免疫组织化学研究来确认。较少

To investigate mechanical effect of repeated minor impact to the pathobiology of the brain, 2 experimental head injury models were designed. In vivo, adult rats were injured utilizing weight-drop device consisting of brass weight(450g) falling through a acrylic guide tube(1m). After 3 insults at an interval of 24 hours, the brain were perfused with 4% Paraformaldehyde in phosphate buffer solution and removed. Histopathological and immunohistochemical studies disclosed neuronal injury in the cerebral cortex, and brain edema in the corpus callosum. Despite the lack of diffuse axonal changes, this model would be suitable for studying neuronal, changes associated with minor head trauma. In vitro model of axonal injury using cultured cells was designed to introduce traumatic alterations on neuronal processes and to identify mechanisms responsible for the formation of focal swellings by observation with phase-contrast and transmission electron microscopes. The culture dishes were oscillated … More one-dimensionally and horizontally 1, 2 or 3 times; repeating at intervals of an hour, 5 seconds a time; on a heat controlled shaker. The amplitude and frequency of the oscillation was 40 mm and 1 Hz, respectively. The injured processes showed two forms: the terminal increase in diameter of the processes and beading depending on injured portions. The microscopic finding suggests that the stress would destroy a cytoskeletal network, and then cause the spherical deformation of the processes. Ultramicroscopically, the beads contained compactly and sparsely misaligned cytoskeletons and prominently gathered densecore vesicles. The cytoskeletal reconstruction within the regenerated growth cones was also noted in the terminal swellings and beads. The destruction of these linkers would be responsible to initiate the cytoskeletal destruction. The initiating point of the cytoskeletal alterations, however, must be confirmed using three dimensional imaging of samples without soluble proteins and immunohistochemical study. Less