Daemen M A, Kurvers H A, Bullens P H, Slaaf D W, Freling G, Kitslaar P J, van den Wildenberg F A
Department of General Surgery, University Hospital Maastricht, The Netherlands.
Neurosci Lett. 1998 May 15;247(2-3):204-8. doi: 10.1016/s0304-3940(98)00304-8.
Loose ligation of a sciatic nerve in rats (chronic constriction injury; CCI) provokes sensory, autonomic, and motor disturbances like those observed in humans with partial peripheral nerve injury. So far, it is unknown whether these motor disturbances result from (mechanical) allodynia or from damage to the motor neuron. These considerations prompted us to assess, in CCI rats, the density of motor axons in both the ligated sciatic nerve and the ipsilateral femoral nerve. To this end, we determined the number of cholinesterase positive fibres. It has been demonstrated previously that muscle fibre type density may be used as a measure of motor denervation and/or hypokinesia. Therefore, the myofibrillar ATPase reaction was employed to assess fibre type density in biopsies obtained from the lateral gastrocnemius muscle (innervated by sciatic nerve) and rectus femoris muscle (innervated by femoral nerve). We observed axonal degeneration of motor fibres within the loosely ligated sciatic nerve, both at an intermediate (day 21) and at a late stage (day 90) after nerve injury. The reduction in the number of motor nerve fibres was more pronounced distal to the site of the ligatures than proximal. A (less pronounced) reduction of motor fibres was observed in the ipsilateral (non-ligated) femoral nerve. In line with these findings, we observed altered fibre type densities in muscle tissue innervated by the ligated sciatic nerve as well as the non-ligated femoral nerve indicative of motor denervation rather than hypokinesia. The findings of this study suggest that the motor disorder induced by partial nerve injury involves degeneration of motor nerve fibres not only within the primarily affected nerve but also within adjacent large peripheral nerves. This spread outside the territory of the primarily affected nerve suggests degeneration of motor neurons at the level of the central nervous system.
在大鼠中对坐骨神经进行松结扎（慢性压迫性损伤；CCI）会引发感觉、自主神经和运动功能障碍，类似于人类部分周围神经损伤时所观察到的情况。到目前为止，尚不清楚这些运动功能障碍是由（机械性）异常性疼痛还是运动神经元损伤引起的。这些考虑促使我们评估CCI大鼠结扎坐骨神经和同侧股神经中运动轴突的密度。为此，我们测定了胆碱酯酶阳性纤维的数量。先前已经证明，肌纤维类型密度可作为运动神经去神经支配和/或运动功能减退的指标。因此，采用肌原纤维ATP酶反应来评估从外侧腓肠肌（由坐骨神经支配）和股直肌（由股神经支配）获取的活检组织中的纤维类型密度。我们观察到，在神经损伤后的中期（第21天）和后期（第90天），松结扎的坐骨神经内运动纤维均发生轴突变性。运动神经纤维数量的减少在结扎部位远端比近端更为明显。在同侧（未结扎）股神经中观察到运动纤维有（不太明显的）减少。与这些发现一致，我们观察到由结扎的坐骨神经以及未结扎的股神经支配的肌肉组织中纤维类型密度发生改变，这表明是运动神经去神经支配而非运动功能减退。本研究结果表明，部分神经损伤所致的运动障碍不仅涉及主要受影响神经内的运动神经纤维变性，还涉及相邻大的周围神经内的运动神经纤维变性。这种在主要受影响神经范围之外的扩散提示中枢神经系统水平的运动神经元变性。
