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神经生长因子通过施万细胞或少突胶质细胞来控制轴突对髓鞘形成的接受能力。

NGF controls axonal receptivity to myelination by Schwann cells or oligodendrocytes.

作者信息

Chan Jonah R, Watkins Trent A, Cosgaya José M, Zhang ChunZhao, Chen Lian, Reichardt Louis F, Shooter Eric M, Barres Ben A

机构信息

Department of Neurobiology, Stanford University School of Medicine, Fairchild Science Building D235, CA 94305, USA.

出版信息

Neuron. 2004 Jul 22;43(2):183-91. doi: 10.1016/j.neuron.2004.06.024.

DOI:10.1016/j.neuron.2004.06.024
PMID:15260955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2758239/
Abstract

Axons dictate whether or not they will become myelinated in both the central and peripheral nervous systems by providing signals that direct the development of myelinating glia. Here we identify the neurotrophin nerve growth factor (NGF) as a potent regulator of the axonal signals that control myelination of TrkA-expressing dorsal root ganglion neurons (DRGs). Unexpectedly, these NGF-regulated axonal signals have opposite effects on peripheral and central myelination, promoting myelination by Schwann cells but reducing myelination by oligodendrocytes. These findings indicate a novel role for growth factors in regulating the receptivity of axons to myelination and reveal that different axonal signals control central and peripheral myelination.

摘要

轴突通过提供指导髓鞘形成性神经胶质细胞发育的信号,决定它们在中枢和外周神经系统中是否会形成髓鞘。在这里,我们确定神经营养因子神经生长因子(NGF)是控制表达TrkA的背根神经节神经元(DRG)髓鞘形成的轴突信号的有效调节因子。出乎意料的是,这些受NGF调节的轴突信号对外周和中枢髓鞘形成有相反的影响,促进雪旺细胞的髓鞘形成,但减少少突胶质细胞的髓鞘形成。这些发现表明生长因子在调节轴突对髓鞘形成的接受性方面具有新作用,并揭示不同的轴突信号控制中枢和外周髓鞘形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/3cb3b747e19a/nihms111845f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/81e8cfe23fbb/nihms111845f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/075e0923dde3/nihms111845f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/6c58fc51a3fa/nihms111845f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/3cb3b747e19a/nihms111845f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/81e8cfe23fbb/nihms111845f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/075e0923dde3/nihms111845f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/6c58fc51a3fa/nihms111845f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/2758239/3cb3b747e19a/nihms111845f4.jpg

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Neurotrophin 3 activation of TrkC induces Schwann cell migration through the c-Jun N-terminal kinase pathway.
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