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C57BL/Wld小鼠外周神经损伤后睫状神经营养因子(CNTF)减少的延迟现象。

Delay of CNTF decrease following peripheral nerve injury in C57BL/Wld mice.

作者信息

Subang M C, Bisby M A, Richardson P M

机构信息

Division of Neurosurgery, Montreal General Hospital and McGill University, Quebec, Canada.

出版信息

J Neurosci Res. 1997 Sep 1;49(5):563-8. doi: 10.1002/(SICI)1097-4547(19970901)49:5<563::AID-JNR6>3.0.CO;2-9.

DOI:10.1002/(SICI)1097-4547(19970901)49:5<563::AID-JNR6>3.0.CO;2-9
PMID:9302077
Abstract

In peripheral nerves, ciliary neurotrophic factor (CNTF) is localized to a subset of Schwann cells and is decreased in synthesis during Wallerian degeneration. This pattern of expression is similar to that of myelin protein genes. In the present study, C57BL/Wld mice, which exhibit delayed Wallerian degeneration, were used to determine the role of axonal contact on the regulation of CNTF synthesis. Western blot analysis showed that CNTF immunoreactivity in Wld nerves remained almost normal even 10 days after ligation when it was almost undetectable in control mice. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that 4 days after ligation, concentrations of CNTF mRNA in Wld mice had decreased much less than in control mice, but that at 10 days CNTF mRNA concentrations in Wld and control mice were comparably low. These observations suggest that maintenance of axonal contact in the absence of axonal transport from the cell body delays the decrease of CNTF mRNA normally seen after injury. Also, during Wallerian degeneration in Wld mice, the decrease of CNTF protein is delayed for many days longer than the decrease in CNTF mRNA.

摘要

在周围神经中,睫状神经营养因子(CNTF)定位于施万细胞的一个亚群,并且在华勒氏变性期间合成减少。这种表达模式与髓磷脂蛋白基因的表达模式相似。在本研究中,利用表现出延迟华勒氏变性的C57BL/Wld小鼠来确定轴突接触在CNTF合成调节中的作用。蛋白质免疫印迹分析表明,即使在结扎后10天,Wld神经中的CNTF免疫反应性仍几乎正常,而在对照小鼠中此时几乎检测不到。逆转录聚合酶链反应(RT-PCR)分析显示,结扎后4天,Wld小鼠中CNTF mRNA的浓度下降程度远小于对照小鼠,但在10天时,Wld小鼠和对照小鼠中CNTF mRNA的浓度相当低。这些观察结果表明,在没有从细胞体进行轴突运输的情况下维持轴突接触会延迟损伤后通常所见的CNTF mRNA的减少。此外,在Wld小鼠的华勒氏变性过程中,CNTF蛋白的减少比CNTF mRNA的减少延迟许多天。

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