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成年大鼠脊髓和大脑皮层横断后酪氨酸激酶受体 C 的表达。

Expression of tyrosine kinase receptor C in the segments of the spinal cord and the cerebral cortex after cord transection in adult rats.

机构信息

Department of Neurosurgery, the Third Affiliated Hospital, Guangzhou Medical College, Guangzhou 510150, China.

出版信息

Neurosci Bull. 2011 Apr;27(2):83-90. doi: 10.1007/s12264-011-1150-1.

Abstract

OBJECTIVE

To investigate the role of tyrosine kinase receptor C (TrkC), the receptor of neurotrophin-3 (NT-3), in neuroplasticity following spinal cord injury (SCI).

METHODS

Rats with cord transection were allowed to survive for 1, 3, 7 and 14 d post operation (dpo). TrkC expressions at lower thoracic levels of the spinal cord and in precentral gyrus of cerebral cortex were investigated.

RESULTS

TrkC protein levels at both the site of injury (T10-T11) and the neighboring segments (T9 and T12) in the spinal cord decreased significantly at 1-7 dpo, followed by a rapid increase at 14 dpo. The temporal changes in TrkC mRNA expression level showed a similar pattern with that of TrkC protein. In addition, the levels of TrkC protein and mRNA at the site of injury (T10-T11) were significantly higher than those at the neighboring spinal segments (T9 and T12). Besides, the levels of TrkC protein and mRNA were higher at the rostral segment than at the caudal segment. However, in the motor cortex, TrkC protein was not detected and TrkC mRNA was expressed at a very low level.

CONCLUSION

These results suggest that TrkC may be involved in neuroplasticity after SCI.

摘要

目的

探讨神经营养因子-3(NT-3)的受体酪氨酸激酶受体 C(TrkC)在脊髓损伤(SCI)后神经重塑中的作用。

方法

对脊髓横断大鼠进行术后 1、3、7 和 14 d 的生存实验,观察脊髓下胸段和大脑皮质运动前区的 TrkC 表达情况。

结果

伤段(T10-T11)及相邻节段(T9 和 T12)脊髓内 TrkC 蛋白水平在术后 1-7 d 显著下降,随后在 14 d 迅速增加。TrkC mRNA 表达水平的时间变化与 TrkC 蛋白相似。此外,伤段(T10-T11)的 TrkC 蛋白和 mRNA 水平明显高于相邻脊髓节段(T9 和 T12)。此外,TrkC 蛋白和 mRNA 的水平在脊髓上段比下段高。然而,在运动皮质中,未检测到 TrkC 蛋白,TrkC mRNA 的表达水平非常低。

结论

这些结果提示 TrkC 可能参与了 SCI 后的神经重塑。

相似文献

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Neurotrophic factors and axonal growth.神经营养因子与轴突生长
Curr Opin Neurobiol. 2002 Oct;12(5):523-31. doi: 10.1016/s0959-4388(02)00372-0.

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