Ochi M, Kwong W H, Kimori K, Chow S P, Ikuta Y
Department of Orthopedic Surgery, Hiroshima University School of Medicine, Japan.
Exp Neurol. 1992 Dec;118(3):291-301. doi: 10.1016/0014-4886(92)90186-t.
We examined whether or not the cervical dorsal root ganglion (DRG) of the rat, when isografted and connected to the distal stump of the severed common peroneal nerve, could survive, project axons to the denervated leg muscles, and exert beneficial influences to delay the degeneration of the denervated muscles. Rats in which the muscles were similarly denervated but no DRG was grafted served as the control. After a postoperative period of 72 to 286 days, histological study showed that nerve cells at the superficial part of the grafted DRG survived. Indirect electrical stimulation via the distal stump of the common peroneal nerve produced no contraction of the muscles, indicating that no functional neuromuscular contacts had been reestablished. Direct stimulation of the denervated muscles did elicit contraction, and the isometric twitch and tetanic tensions were significantly much higher in the experimental rats with a grafted DRG than in the control rats. Cholinesterase-silver staining indicated the presence of axons in the denervated muscles, but the axons did not terminate on endplates. Compared with the control muscles, the experimental muscles had significantly more axons, and had atrophied less as indicated by muscle wet weight and histological appearance. These results indicate that the sensory axons can delay the weakening and atrophy of muscles after denervation. We suggest that the sensory axons may exert certain trophic influence on the denervated muscle fibers, though the actual mechanism is unknown.
我们研究了大鼠颈背根神经节(DRG)在同种异体移植并连接到切断的腓总神经远端残端后,是否能够存活,将轴突投射到失神经支配的腿部肌肉,并发挥有益作用以延缓失神经支配肌肉的退化。将肌肉同样失神经支配但未移植DRG的大鼠作为对照。术后72至286天,组织学研究表明移植的DRG浅层的神经细胞存活。通过腓总神经远端残端进行间接电刺激未引起肌肉收缩,表明未重新建立功能性神经肌肉联系。直接刺激失神经支配的肌肉确实引起了收缩,并且移植了DRG的实验大鼠的等长收缩和强直张力明显高于对照大鼠。胆碱酯酶银染色表明失神经支配的肌肉中有轴突存在,但轴突未终止于终板。与对照肌肉相比,实验肌肉中的轴突明显更多,并且从肌肉湿重和组织学外观来看萎缩程度较小。这些结果表明感觉轴突可以延缓失神经支配后肌肉的减弱和萎缩。我们认为感觉轴突可能对失神经支配的肌纤维发挥某种营养作用,尽管实际机制尚不清楚。