Active endocytosis and microtubule remodeling restore compressed pyramidal neuron morphology in rat cerebral cortex

主动内吞作用和微管重塑可恢复大鼠大脑皮层中受压锥体神经元的形态

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Abstract

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.

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