Waters H J, Barnett G, O'Hanlon G M, Lowrie M B
Division of Biomedical Sciences, Imperial College School of Medicine, Norfolk Place, London, W2 1PG, United Kingdom.
Exp Neurol. 1998 Jul;152(1):95-100. doi: 10.1006/exnr.1998.6820.
Sciatic nerve crush at birth results in the death of most of the motoneurons in the sciatic motor pool. It has been proposed that these cells die through excessive activation which can be explained partly by an increased susceptibility to NMDA. However, it is also possible that decreased inhibitory mechanisms resulting from nerve injury may contribute to overactivation of the motoneurons. In this study we compared the survival of motoneurons innervating two muscles in the peroneal motor pool, tibialis anterior and extensor digitorum longus, after either sciatic or common peroneal nerve crush. These two procedures both axotomize the motoneurons but differ in their effects on afferent input. Sciatic nerve crush severely reduces the afferent input from the antagonist muscles innervated via the tibial nerve, whereas common peroneal nerve crush preserves them. Using retrograde labeling with horseradish peroxidase, we found that almost twice as many motoneurons survived common peroneal nerve crush than sciatic nerve crush and that muscle weight showed a corresponding significant improvement. A control experiment excluded the possible involvement of increased stretch of the muscles as a result of common peroneal nerve crush alone as an explanation for the improvement. We therefore suggest that the increased survival of motoneurons after peroneal nerve crush was due to the preservation of their reciprocal inhibitory input. However, since even with this improvement the majority of motoneurons still died, loss of reciprocal inhibition probably does not play a major role in the death of motoneurons induced by overactivation.
出生时坐骨神经挤压会导致坐骨运动神经元池中大多数运动神经元死亡。有人提出，这些细胞因过度激活而死亡，这可以部分地通过对N-甲基-D-天冬氨酸（NMDA）敏感性增加来解释。然而，神经损伤导致的抑制机制减弱也可能导致运动神经元过度激活。在本研究中，我们比较了坐骨神经或腓总神经挤压后，支配腓总运动神经元池中的两块肌肉（胫骨前肌和趾长伸肌）的运动神经元的存活情况。这两种操作都会使运动神经元发生轴突切断，但对传入输入的影响不同。坐骨神经挤压会严重减少通过胫神经支配的拮抗肌的传入输入，而腓总神经挤压则能保留这些传入输入。使用辣根过氧化物酶逆行标记，我们发现腓总神经挤压后存活的运动神经元数量几乎是坐骨神经挤压后的两倍，并且肌肉重量也有相应的显著改善。一项对照实验排除了仅因腓总神经挤压导致肌肉拉伸增加作为改善原因的可能性。因此，我们认为腓总神经挤压后运动神经元存活率增加是由于保留了它们的相互抑制性输入。然而，即使有这种改善，大多数运动神经元仍然死亡，相互抑制的丧失可能在过度激活诱导的运动神经元死亡中不发挥主要作用。
