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APS -APS March Meeting 2017 - Event - Neurofilament kinetics and changes in axonal caliber after axonal injury

机译:APS -APS 2017年3月会议-事件-轴突损伤后神经丝动力学和轴突口径变化

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Neurofilaments (NF) are the most abundant cytoskeletal structures in neuronal axons and determine their caliber. NFs are assembled in the cell body, and are also cargo of slow axonal transport moving distally at rate of 0.1 -- 1 mm/day.This dual role of NFs, as space filling structures and cargo of slow transport, im-plies a complex relation between axon caliber, NF influx from the cell body and transport kinetics, which is subject of our research. Changes in axon caliber, NF velocity, and NF flux observed after axonal injury, presents a good model system to study these complex relations. Axonal injury signals the cell body to reduce NF and tubulin influx, resulting in a wave of axon thinning, propagating distally at a rate consistent with NF velocity, while at the same time, NF transport rate is in- creasing. We developed a novel computational model for NF transport, where ac- cess of NFs to microtubule tracks and their organization determines their motility. Using this new computational model, we can relate the time-course of post-injury axonal thinning and increase of NF velocity by a reduction of NF flux and tubulin. The subsequent time - course of axonal recovery can be likewise associated with a recovery of NF flux and tubulin abundance.
机译:神经丝(NF)是神经元轴突中最丰富的细胞骨架结构,并决定其口径。 NFs组装在细胞体内,并且也是轴突运输缓慢的货物,以0.1-1 mm / day的速率向远侧移动.NFs的双重作用是空间填充结构和运输缓慢的货物,意味着复杂轴突口径,NF从细胞体内的流入与运输动力学之间的关系,这是我们研究的主题。轴突损伤后观察到的轴突口径,NF速度和NF通量的变化,为研究这些复杂的关系提供了一个很好的模型系统。轴突损伤提示细胞体减少NF和微管蛋白流入,导致轴突变薄,以与NF速度一致的速率向远侧传播,与此同时,NF转运速率增加。我们开发了一种新型的NF转运计算模型,其中NF进入微管轨道及其组织决定了它们的运动能力。使用这个新的计算模型,我们可以通过减少NF通量和微管蛋白来联系损伤后轴突变薄和NF速度增加的时间过程。随后的轴突恢复时间-过程也可以与NF通量和微管蛋白丰度的恢复相关。

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