Martini R, Mohajeri M H, Kasper S, Giese K P, Schachner M
Department of Neurobiology, Swiss Federal Institute of Technology, Zürich.
J Neurosci. 1995 Jun;15(6):4488-95. doi: 10.1523/JNEUROSCI.15-06-04488.1995.
In search for the molecular mechanisms underlying the formation of the major dense line in peripheral nerve myelin we investigated mice deficient in the myelin proteins P0 and MBP. In mice lacking both molecules axons were enwrapped by myelin-like processes devoid of the major dense line, while mice deficient in either protein showed, respectively, partial and normal compaction. Mice heterozygous for P0 but devoid of MBP showed myelin of reduced thickness around axons of normal caliber. Both molecules thus contribute to the formation of the major dense line and to the determination of myelin thickness. Furthermore, our observations modify the view that axon caliber is dependent on normal myelin.
为了探寻周围神经髓鞘中主致密线形成的分子机制，我们研究了髓鞘蛋白P0和髓鞘碱性蛋白（MBP）缺失的小鼠。在这两种分子均缺乏的小鼠中，轴突被缺乏主致密线的髓鞘样突起所包裹，而仅缺乏其中一种蛋白的小鼠则分别表现出部分致密化和正常致密化。P0基因杂合但缺乏MBP的小鼠，其正常管径轴突周围的髓鞘厚度减小。因此，这两种分子均有助于主致密线的形成以及髓鞘厚度的确定。此外，我们的观察结果改变了轴突管径依赖于正常髓鞘这一观点。
