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神经损伤会增加发育中大鼠运动神经元对N-甲基-D-天冬氨酸诱导的神经毒性的易感性。

Nerve injury increases the susceptibility of motoneurons to N-methyl-D-aspartate-induced neurotoxicity in the developing rat.

作者信息

Greensmith L, Hasan H I, Vrbová G

机构信息

Department of Anatomy and Developmental Biology, University College, London, U.K.

出版信息

Neuroscience. 1994 Feb;58(4):727-33. doi: 10.1016/0306-4522(94)90450-2.

DOI:10.1016/0306-4522(94)90450-2
PMID:7910669
Abstract

If the sciatic nerve is crushed in neonatal rats, a large proportion of motoneurons die, but the same injury inflicted at five days of age results in little, if any, motoneuron death. However, these motoneurons are rendered susceptible to the excitotoxic effects of the glutamate agonist, N-methyl-D-aspartate. Retrograde labelling of soleus motoneurons after nerve crush at five days of age, followed by treatment with N-methyl-D-aspartate seven days later, shows that only 36 +/- 7.5% of motoneurons have survived. If the motoneurons are allowed to reinnervate their target, and N-methyl-D-aspartate is applied three weeks after the nerve injury, no motoneuron death is observed. Furthermore, adult motoneurons remain resistant to the toxic effects of N-methyl-D-aspartate, even after nerve injury. These results indicate that glutamate, the main excitatory neurotransmitter in the developing spinal cord, may be involved in the motoneuron death that occurs following nerve injury during early postnatal development.

摘要

如果在新生大鼠中坐骨神经被挤压,很大一部分运动神经元会死亡,但在出生五天时遭受同样的损伤,即使有运动神经元死亡,数量也极少。然而,这些运动神经元会变得易受谷氨酸激动剂N-甲基-D-天冬氨酸的兴奋毒性作用影响。在出生五天时对比目鱼肌运动神经元进行神经挤压后逆行标记,七天后用N-甲基-D-天冬氨酸处理,结果显示只有36±7.5%的运动神经元存活下来。如果让运动神经元重新支配它们的靶标,并在神经损伤三周后应用N-甲基-D-天冬氨酸,则未观察到运动神经元死亡。此外,即使在神经损伤后,成年运动神经元对N-甲基-D-天冬氨酸的毒性作用仍具有抗性。这些结果表明,谷氨酸作为发育中的脊髓中的主要兴奋性神经递质,可能与出生后早期发育期间神经损伤后发生的运动神经元死亡有关。

相似文献

1
Nerve injury increases the susceptibility of motoneurons to N-methyl-D-aspartate-induced neurotoxicity in the developing rat.神经损伤会增加发育中大鼠运动神经元对N-甲基-D-天冬氨酸诱导的神经毒性的易感性。
Neuroscience. 1994 Feb;58(4):727-33. doi: 10.1016/0306-4522(94)90450-2.
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Over-expression of parvalbumin in transgenic mice rescues motoneurons from injury-induced cell death.在转基因小鼠中过表达小白蛋白可使运动神经元免受损伤诱导的细胞死亡。
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Neuroscience. 1998 Sep;86(1):291-9. doi: 10.1016/s0306-4522(98)00037-2.

引用本文的文献

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BMC Physiol. 2012 May 2;12:5. doi: 10.1186/1472-6793-12-5.
2
Induction of reactive astrocytosis and prevention of motoneuron cell death by the I(2)-imidazoline receptor ligand LSL 60101.I(2)-咪唑啉受体配体LSL 60101诱导反应性星形细胞增生并预防运动神经元细胞死亡
Br J Pharmacol. 2000 Aug;130(8):1767-76. doi: 10.1038/sj.bjp.0703485.
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Regulation of ion channel expression in neural cells by hormones and growth factors.
激素和生长因子对神经细胞中离子通道表达的调节。
Mol Neurobiol. 1998 Dec;18(3):175-225. doi: 10.1007/BF02741300.