Institute of Pathophysiology, Zaloška 4, 61000 Ljubljana, Slovenia.
Restor Neurol Neurosci. 1994 Jan 1;7(2):89-94. doi: 10.3233/RNN-1994-7204.
We investigated if continuous 1 µA direct current stimulation of the injured nerve, with the cathode electrode at the distal end of the nerve crush injury (cathode stimulation), accelerated the recovery of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity in transiently denervated extensor digitorum longus (EDL) and soleus (SOL) rat muscles. ChAT is a specific marker of cholinergic nerve terminals and may reflect axon ingrowth, and AChE reflects the re-establishment of neuromuscular junctions and recovery of muscle activity. Compared to sham operated animals, the cathode (CA) stimulated rats had a statistically significant larger ChAT activity in the EDL and SOL muscles on days 12 and 14 after nerve crush (P < 0.01, n = 6). The difference in ChAT activity between the groups decreased thereafter. Regarding recovery of muscle AChE, CA stimulation of the crushed sciatic nerve did not detectably accelerate the normalization of activity and pattern of AChE molecular forms in the EDL and SOL muscles. This means that the early rise in ChAT muscle activity in CA stimulated rats was not followed by an accelerated normalization of the neuromuscular transmission in the same group. It is more likely that the higher ChAT activity observed after cathode stimulation indicates a higher ChAT content in regenerating motor nerve endings, rather than a greater number of motor axons entering the muscles. It seems possible that cathode stimulation increased ChAT axonal transport, causing the early increase of ChAT content in the nerve endings. This raises the possibility that the axon transport and subsequent secretion of a trophic factor(s) from the nerve to the reinnervated muscle are enhanced as well, thus shortening the overall time of muscle force recovery in the absence of an appreciable acceleration of recovery of the neuromuscular transmission.
我们研究了持续 1 µA 的直流电刺激损伤神经，阴极电极位于神经挤压伤的远端（阴极刺激），是否能加速短暂去神经的伸趾长肌（EDL）和比目鱼肌（SOL）大鼠肌肉中胆碱乙酰转移酶（ChAT）和乙酰胆碱酯酶（AChE）活性的恢复。ChAT 是胆碱能神经末梢的特异性标志物，可能反映轴突的生长，AChE 反映运动终板的重建和肌肉活动的恢复。与假手术动物相比，在神经挤压后 12 天和 14 天，阴极（CA）刺激大鼠的 EDL 和 SOL 肌肉中的 ChAT 活性有统计学意义的增加（P < 0.01，n = 6）。此后，两组之间的 ChAT 活性差异减小。关于肌肉 AChE 的恢复，CA 刺激挤压的坐骨神经并没有明显加速 EDL 和 SOL 肌肉中 AChE 分子形式的正常化。这意味着 CA 刺激大鼠肌肉中 ChAT 活性的早期升高并没有伴随着同一组神经肌肉传递的加速正常化。更有可能的是，阴极刺激后观察到的 ChAT 活性升高表明再生运动神经末梢中的 ChAT 含量更高，而不是更多的运动轴突进入肌肉。阴极刺激可能增加了 ChAT 轴突运输，导致神经末梢中 ChAT 含量的早期增加，这增加了神经向再支配肌肉中输送营养因子（s）的轴突运输和随后分泌的可能性，从而缩短了肌肉力量恢复的总时间，而没有明显加速神经肌肉传递的恢复。
