Department of Anatomy, Tzu Chi University, Hualien, Taiwan.
Cell Mol Neurobiol. 2012 Oct;32(7):1079-87. doi: 10.1007/s10571-012-9831-5. Epub 2012 Mar 30.
Previous studies have shown that compression alone reduced the thickness of rat cerebral cortex and apical dendritic lengths of pyramidal neurons without apparent cell death. Besides, decompression restored dendritic lengths at different degrees depending on duration of compression. To understand the mechanisms regulating dendritic shortening and lengthening upon compression and decompression, we applied transmission electron microscopy to examine microtubule and membrane structure of pyramidal neurons in rat sensorimotor cortex subjected to compression and decompression. Microtubule densities within apical dendritic trunks decreased significantly and arranged irregularly following compression for a period from 30 min to 24 h. In addition, apical dendritic trunks showed twisted contour. Two reasons are accounted for the decrease of microtubule density within this period. First, microtubule depolymerized and resulted in lower number of microtubules. Second, the twisted membrane widened the diameters of apical dendritic trunks, which also caused a decrease in microtubule density. Interestingly, these compression-induced changes were quickly reversed to control level following decompression, suggesting that these changes were accomplished passively. Furthermore, microtubule densities were restored to control level and the number of endocytotic vesicles significantly increased along the apical dendritic membrane in neurons subjected to 36 h or longer period of compression. However, decompression did not make significant changes on dendrites compressed for 36 h, for they had already shown straight appearance before decompression. These results suggest that active membrane endocytosis and microtubule remodeling occur in this adaptive stage to make the apical dendritic trunks regain their smooth contour and regular microtubule arrangement, similar to that of the normal control neurons.
先前的研究表明，单纯的压迫即可减少大脑皮质的厚度和锥体神经元的树突顶长度，而没有明显的细胞死亡。此外，减压在不同程度上恢复了树突长度，这取决于压迫的持续时间。为了了解调节压迫和减压时树突缩短和延长的机制，我们应用透射电子显微镜检查了大鼠感觉运动皮层中受压和解压的锥体神经元的微管和膜结构。在受压 30 分钟至 24 小时期间，树突顶干内的微管密度显著降低且排列不规则。此外，树突顶干呈现扭曲的轮廓。在这段时间内微管密度降低有两个原因。首先，微管解聚导致微管数量减少。其次，扭曲的膜扩大了树突顶干的直径，这也导致微管密度降低。有趣的是，这些压迫引起的变化在减压后很快恢复到对照水平，表明这些变化是被动完成的。此外，在受压 36 小时或更长时间的神经元中，微管密度恢复到对照水平，并且沿树突顶膜的内吞小泡数量显著增加。然而，对于受压 36 小时的树突，减压没有产生显著变化，因为在减压之前它们已经呈现出笔直的外观。这些结果表明，在这个适应阶段发生了主动的膜内吞作用和微管重塑，以使树突顶干恢复其平滑轮廓和规则的微管排列，类似于正常对照神经元。
