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Influence of non-neuronal cells on regeneration of the rat sciatic nerve.

作者信息

Sjöberg J, Kanje M, Edström A

机构信息

Department of Zoophysiology, University of Lund, Sweden.

出版信息

Brain Res. 1988 Jun 21;453(1-2):221-6. doi: 10.1016/0006-8993(88)90161-8.

DOI:10.1016/0006-8993(88)90161-8
PMID:3401760
Abstract

The ability of the rat sciatic nerve to regenerate into a previously frozen distal nerve segment was studied and compared to regeneration after a crush lesion. The regeneration rate in the frozen segment was 1.9 mm/day, which was approximately half of that observed after a crush lesion (3.3 mm/day). If an unfrozen nerve segment was left intact beyond the frozen section, the rate of regeneration increased to 3.2 mm/day. However, a fresh nerve segment sutured along the frozen segment did not significantly affect the rate of regeneration. Incorporation of [3H]thymidine in the regenerating nerve, analyzed after 1, 3 and 6 days, showed an increased labelling in the frozen segment. This increase spread from the proximal nerve segment into the frozen section. In nerves where a segment was left intact beyond the frozen section, [3H]thymidine incorporation was seen to enter the frozen section from both sides. The spreading of [3H]thymidine incorporation appeared to correlate with the rate of regeneration. However, the same pattern of incorporation could be observed in nerves where regeneration was detained by a transection. The results suggest that Schwann and/or other cells which invade the frozen nerve segment affect the rate of axonal elongation, and that the migration of these cells occurs independently of regenerating fibers.

摘要

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Axonal outgrowth is associated with increased ERK 1/2 activation but decreased caspase 3 linked cell death in Schwann cells after immediate nerve repair in rats.轴突生长与 ERK1/2 激活增加有关,但在大鼠即时神经修复后,雪旺细胞中的 caspase 3 相关细胞死亡减少。
BMC Neurosci. 2011 Jan 21;12:12. doi: 10.1186/1471-2202-12-12.
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坐骨神经损伤预处理后体外神经突再生增强的机制。
J Comp Neurol. 1998 Feb 2;391(1):11-29. doi: 10.1002/(sici)1096-9861(19980202)391:1<11::aid-cne2>3.0.co;2-u.
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