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髓鞘相关糖蛋白基因的破坏改善了C57BL/Wlds小鼠中轴突沿髓鞘的再生。

Disruption of the gene for the myelin-associated glycoprotein improves axonal regrowth along myelin in C57BL/Wlds mice.

作者信息

Schäfer M, Fruttiger M, Montag D, Schachner M, Martini R

机构信息

Department of Neurobiology, Swiss Federal Institute of Technology, Zürich, Switzerland.

出版信息

Neuron. 1996 Jun;16(6):1107-13. doi: 10.1016/s0896-6273(00)80137-3.

Abstract

The myelin-associated glycoprotein (MAG) has been shown to be inhibitory for certain neurons in vitro (Mukhopadhyay et al., 1994; McKerracher et al., 1994). To investigate whether MAG is an inhibitory component in peripheral myelin in vivo, MAG-deficient mutant mice were cross-bred with C57BL/Wlds mice that have delayed lesion-induced myelin degeneration and axon regrowth. While in crushed nerves of C57BL/Wlds mice expressing MAG, only 16% of myelin sheaths were associated with regrowing axons, this number was doubled in MAG-deficient C57BL/Wlds mice. These observations suggest that the absence of MAG may contribute to the improved axonal regrowth in the double mutants. Therefore, degeneration of MAG-containing myelin might be an important prerequisite to optimize axonal regrowth after peripheral nerve injury.

摘要

髓鞘相关糖蛋白(MAG)已被证明在体外对某些神经元具有抑制作用(Mukhopadhyay等人,1994年;McKerracher等人,1994年)。为了研究MAG在体内是否是外周髓鞘中的抑制成分,将MAG缺陷型突变小鼠与具有延迟损伤诱导的髓鞘变性和轴突再生的C57BL/Wlds小鼠进行杂交。在表达MAG的C57BL/Wlds小鼠的挤压神经中,只有16%的髓鞘与再生轴突相关,而在MAG缺陷的C57BL/Wlds小鼠中,这一数字增加了一倍。这些观察结果表明,MAG的缺失可能有助于双突变体中轴突再生的改善。因此,含MAG的髓鞘变性可能是优化外周神经损伤后轴突再生的重要前提条件。

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