Myelin-associated glycoprotein is a myelin signal that modulates the caliber of myelinated axons
Myelin-associated glycoprotein is a myelin signal that modulates the caliber of myelinated axons
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DOI：
10.1523/jneurosci.18-06-01953.1998
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发表时间：
1998-03-15
影响因子：
5.3
通讯作者：
Trapp, BD
中科院分区：
文献类型：
--
作者：
Yin, XH;Crawford, TO;Trapp, BD
髓鞘形成通过其绝缘特性和增加轴突口径的未知外在效应来增加神经元传导速度。尽管众所周知脱髓鞘可导致轴突萎缩，但调节轴突口径的髓磷脂分子尚不清楚。致密周围神经系统 (PNS) 髓磷脂、P-o 蛋白和髓磷脂碱性蛋白结构蛋白的丢失不会导致轴突萎缩。这项研究表明，髓鞘相关糖蛋白 (MAG) 基因无效突变的小鼠有髓鞘 PNS 轴突慢性萎缩，导致结节旁髓鞘和轴突变性。 MAG 的缺失与轴突口径减小、神经丝间距减小和神经丝磷酸化减少相关。由于 MAG 缺陷小鼠的轴突萎缩和变性是在没有炎症、髓鞘形成不足、显着脱髓鞘-髓鞘再生或功能突变获得的情况下发生的，因此这些数据支持 MAG 在调节有髓轴突的成熟和活力方面的功能作用。
Myelination increases neuronal conduction velocity through its insulating properties and an unidentified extrinsic effect that increases axonal caliber. Although it is well established that demyelination can cause axonal atrophy, the myelin molecule that regulates axonal caliber is not known. Loss of the structural proteins of compact peripheral nervous system (PNS) myelin, P-o protein, and myelin basic protein does not lead to axonal atrophy. This study demonstrates that mice with a null mutation of the myelin-associated glycoprotein (MAG) gene have a chronic atrophy of myelinated PNS axons that results in paranodal myelin tomaculi and axonal degeneration. Absence of MAG was correlated with reduced axonal calibers, decreased neurofilament spacing, and reduced neurofilament phosphorylation. Because axonal atrophy and degeneration in MAG-deficient mice occur in the absence of inflammation, hypomyelination, significant demyelination-remyelination, or gain of function mutations, these data support a functional role for MAG in modulating the maturation and viability of myelinated axons.