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新生大鼠坐骨神经损伤后,给予镁可促进运动单位存活。

Magnesium administration provokes motor unit survival, after sciatic nerve injury in neonatal rats.

作者信息

Gougoulias N, Hatzisotiriou A, Kapoukranidou D, Albani M

机构信息

Royal Cornwall Hospital, Treslike, Truto- Cornwall, TR1 3LL, United Kingdom.

出版信息

BMC Musculoskelet Disord. 2004 Sep 24;5(1):33. doi: 10.1186/1471-2474-5-33.

Abstract

BACKGROUND

We examined the time course of the functional alterations in two types of muscles following sciatic nerve crush in neonatal rats and the neuroprotective effect of Mg2+.

METHODS

The nerve crush was performed on the 2nd postnatal day. MgSO4*7H2O was administered daily for two weeks. Animals were examined for the contractile properties and for the number of motor units of extensor digitorum longus and soleus muscles at three postnatal stages and adulthood. Four experimental groups were included in this study: i) controls, ii) axotomized rats, iii) magnesium treated controls and iv) axotomized and Mg2+-treated rats.

RESULTS

Axotomy resulted in 20% MU survival in EDL and 50% in soleus. In contrast, magnesium treatment resulted in a significant motor unit survival (40% survival in EDL and 80% in soleus). The neuroprotective effects of Mg2+ were evident immediately after the Mg2+-treatment. Immature EDL and soleus muscles were slow and fatigueable. Soleus gradually became fatigue resistant, whereas, after axotomy, soleus remained fatigueable up to adulthood. EDL gradually became fastcontracting. Tetanic contraction in axotomized EDL was just 3,3% of the control side, compared to 15,2% in Mg2+-treated adult rats. The same parameter for axotomized soleus was 12% compared to 97% in Mg2+-treated adult rats.

CONCLUSIONS

These results demonstrate that motoneuron death occurs mostly within two weeks of axotomy. Magnesium administration rescues motoneurons and increases the number of motor units surviving into adulthood. Fast and slow muscles respond differently to axotomy and to subsequent Mg2+ treatment in vivo.

摘要

背景

我们研究了新生大鼠坐骨神经损伤后两种类型肌肉功能改变的时间进程以及镁离子(Mg2+)的神经保护作用。

方法

在出生后第2天进行神经损伤。每天给予MgSO4·7H2O,持续两周。在出生后的三个阶段及成年期对动物的趾长伸肌和比目鱼肌的收缩特性和运动单位数量进行检查。本研究包括四个实验组:i)对照组,ii)轴突切断的大鼠,iii)镁处理的对照组,iv)轴突切断并经Mg2+处理的大鼠。

结果

轴突切断导致趾长伸肌中20%的运动单位存活,比目鱼肌中50%的运动单位存活。相比之下,镁处理导致运动单位显著存活(趾长伸肌中40%存活,比目鱼肌中80%存活)。Mg2+处理后立即显现出神经保护作用。未成熟的趾长伸肌和比目鱼肌收缩缓慢且易疲劳。比目鱼肌逐渐变得抗疲劳,而轴突切断后,比目鱼肌直至成年仍易疲劳。趾长伸肌逐渐变为快速收缩。轴突切断的趾长伸肌的强直收缩仅为对照侧的3.3%,而在经Mg2+处理的成年大鼠中为15.2%。轴突切断的比目鱼肌的相同参数为12%,而在经Mg2+处理的成年大鼠中为97%。

结论

这些结果表明运动神经元死亡大多发生在轴突切断后的两周内。给予镁可挽救运动神经元并增加存活至成年期的运动单位数量。快肌和慢肌在体内对轴突切断及随后的Mg2+处理反应不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7665/522819/735fd91bb583/1471-2474-5-33-1.jpg

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