Pellegrino R G, Spencer P S
Brain Res. 1985 Aug 19;341(1):16-25. doi: 10.1016/0006-8993(85)91467-2.
Schwann cell mitosis has been demonstrated in chronically denervated cat tibial nerves re-innervated by axons regenerating from the proximal stump of a coapted peroneal nerve. Thymidine incorporation rose above baseline levels at the axon front, with no detectable increase in more distal regions occupied by denervated Schwann cells. Schwann cells therefore enter S phase upon the arrival of a regenerating axon in vivo as previously described in tissue culture. Intraneural treatment of the denervated distal stump with Mitomycin C prior to re-innervation delayed the subsequent appearance of myelin formation. This supports the notion that axonally stimulated division of Schwann cells is a prerequisite for myelination during nerve regeneration. Axonal advancement was also retarded by drug treatment, possibly because of a reduced level of trophic support provided by the compromised Schwann cells. A comparable absence of myelin and poor re-innervation was found in chemically untreated distal stumps that had been maintained in the denervated state for prolonged periods when Schwann cell columns are known to undergo progressive atrophy. These observations suggest that nerve repair should be delayed for limited periods if efficacious regeneration is desired.
在由吻合的腓总神经近端残端再生的轴突重新支配的慢性失神经支配的猫胫神经中，已证实施万细胞有丝分裂。在轴突前端，胸苷掺入量高于基线水平，而在由失神经支配的施万细胞占据的更远端区域未检测到增加。因此，如先前在组织培养中所描述的，施万细胞在体内再生轴突到达时进入S期。在重新支配之前，用丝裂霉素C对失神经支配的远端残端进行神经内治疗会延迟随后髓鞘形成的出现。这支持了这样一种观点，即轴突刺激的施万细胞分裂是神经再生过程中髓鞘形成的先决条件。药物治疗也会阻碍轴突的推进，这可能是由于受损的施万细胞提供的营养支持水平降低所致。在已知施万细胞柱会发生进行性萎缩的情况下，在长期保持失神经支配状态的未经化学处理的远端残端中，也发现了类似的髓鞘缺失和重新支配不良的情况。这些观察结果表明，如果希望实现有效的再生，神经修复应延迟有限的时间。
