Elder G A, Friedrich V L, Lazzarini R A
Department of Psychiatry, Mount Sinai School of Medicine, New York, New York 10029, USA.
J Neurosci Res. 2001 Sep 15;65(6):493-9. doi: 10.1002/jnr.1179.
Schwann cells and oligodendrocytes produce myelin sheaths of widely varying sizes. How these cells determine the size of myelin sheath for a particular axon is incompletely understood. Axonal diameter has long been suspected to be a signal in this process. We have analyzed myelin sheath thickness in L5 lumbar root and spinal cord white matter of a series of mouse mutants with diminished axonal calibers resulting from a deficiency of neurofilaments (NFs). In the PNS, average axonal diameters were reduced by 20-37% in the NF mutants. Remarkably, the average myelin sheath thickness remained unchanged from control values, and regression analysis showed sheaths abnormally thick for a given size of axon. These data show that a genetically induced reduction in axonal caliber does not cause a reduction in myelin sheath thickness in PNS and indicate that Schwann cells read some intrinsic signal on axons that can be uncoupled from axonal diameter. Interestingly, myelin sheaths in the spinal cord of these animals were not abnormally thick, arguing that axonal diameter may contribute directly to the regulation of myelination in the CNS and that oligodendrocytes and Schwann cells use different cues to set myelin sheath thickness.
施万细胞和少突胶质细胞产生大小差异很大的髓鞘。这些细胞如何确定特定轴突的髓鞘大小尚未完全清楚。长期以来，人们一直怀疑轴突直径是这一过程中的一个信号。我们分析了一系列因神经丝（NF）缺乏导致轴突直径减小的小鼠突变体的L5腰神经根和脊髓白质中的髓鞘厚度。在周围神经系统（PNS）中，NF突变体的平均轴突直径减少了20%-37%。值得注意的是，平均髓鞘厚度与对照值相比保持不变，回归分析表明，对于给定大小的轴突，髓鞘异常增厚。这些数据表明，基因诱导的轴突直径减小不会导致PNS中髓鞘厚度的减小，并表明施万细胞读取轴突上一些可与轴突直径解耦的内在信号。有趣的是，这些动物脊髓中的髓鞘并不异常增厚，这表明轴突直径可能直接参与中枢神经系统（CNS）髓鞘形成的调节，并且少突胶质细胞和施万细胞使用不同的线索来设定髓鞘厚度。
