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周围神经移植物植入可抑制神经元型一氧化氮合酶的诱导,并提高神经根撕脱后脊髓运动神经元的存活率。

Implantation of PNS graft inhibits the induction of neuronal nitric oxide synthase and enhances the survival of spinal motoneurons following root avulsion.

作者信息

Wu W, Han K, Li L, Schinco F P

机构信息

Department of Neurosurgery, Eastern Virginia Medical School, Norfolk 23501.

出版信息

Exp Neurol. 1994 Oct;129(2):335-9. doi: 10.1006/exnr.1994.1176.

DOI:10.1006/exnr.1994.1176
PMID:7525335
Abstract

In a spinal root injury model, our previous studies have shown that induction of nitric oxide synthase (NOS) appears only in spinal motoneurons of the root-avulsed segment in which significant motoneuron loss occurs but not in those of the distal root-axotomized segment (root axotomy 5-10 mm from the spinal cord) in which most motoneurons survive the injury. One hypothesis for the different response of motoneurons to root avulsion and distal root axotomy is that neurotrophic factors produced by the remaining peripheral nervous system (PNS) component are available for the distally axotomized motoneurons but are not available following avulsion. This hypothesis is tested in the present study by implantation of a PNS graft following the root avulsion. Results of the present study show that implantation of a PNS graft significantly enhances the survival of motoneurons following avulsion. Expression of NOS due to avulsion injury is completely inhibited in all motoneurons that regrow into the PNS graft. These results indicate that induction of NOS in avulsed motoneurons may result from the deprivation of neurotrophic factors produced by the PNS component, and the survival promoting effects of neurotrophic factors may be achieved by modifying certain cellular molecules such as NOS.

摘要

在一个脊神经根损伤模型中,我们之前的研究表明,一氧化氮合酶(NOS)的诱导仅出现在神经根撕脱节段的脊髓运动神经元中,该节段会发生明显的运动神经元丢失,而在远端神经根切断节段(距脊髓5 - 10毫米的神经根切断)的运动神经元中则不会出现,在该节段大多数运动神经元在损伤后存活。运动神经元对神经根撕脱和远端神经根切断有不同反应的一种假设是,剩余外周神经系统(PNS)成分产生的神经营养因子可被远端切断轴突的运动神经元利用,但在神经根撕脱后则无法利用。本研究通过在神经根撕脱后植入PNS移植物来检验这一假设。本研究结果表明,植入PNS移植物可显著提高神经根撕脱后运动神经元的存活率。在所有长入PNS移植物的运动神经元中,由撕脱损伤引起的NOS表达被完全抑制。这些结果表明,撕脱的运动神经元中NOS的诱导可能是由于PNS成分产生的神经营养因子被剥夺所致,并且神经营养因子的存活促进作用可能通过修饰某些细胞分子如NOS来实现。

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