Martini R
Department of Neurology, Section of Developmental Neurobiology, University of Würzburg, Josef-Schneider-Strasse 11, D-97080 Würzburg, Germany.
Muscle Nerve. 2001 Apr;24(4):456-66. doi: 10.1002/mus.1027.
Myelinating Schwann cells control the number of neurofilaments and elevate the phosphorylation state of neurofilaments in the axon, eventually leading to the typical large axon caliber. Conversely, absence of myelin leads to lower amounts of neurofilaments, reduced phosphorylation levels, and smaller axon diameters. In addition, myelinating Schwann cells mediate the spacing of Na(+) channel clusters during development of the node of Ranvier. When axons are associated with mutant Schwann cells in inherited neuropathies, their calibers are reduced and their neurofilaments are less phosphorylated and more closely spaced. Also, axonal transport is reduced and axons degenerate at the distal ends of long nerves. Myelin-associated glycoprotein may mediate some aspects of Schwann cell-axon communication, but much remains to be learned about the molecular bases of Schwann cell-axon communication.
形成髓鞘的施万细胞控制神经丝的数量，并提高轴突中神经丝的磷酸化状态，最终导致典型的大轴突管径。相反，缺乏髓鞘会导致神经丝数量减少、磷酸化水平降低以及轴突直径变小。此外，在郎飞结发育过程中，形成髓鞘的施万细胞介导钠通道簇的间距。当轴突在遗传性神经病变中与突变的施万细胞相关联时，它们的管径减小，神经丝磷酸化程度降低且间距更近。而且，轴突运输减少，轴突在长神经远端发生退化。髓鞘相关糖蛋白可能介导施万细胞与轴突通讯的某些方面，但关于施万细胞与轴突通讯的分子基础仍有许多有待了解之处。
