Knyihár E, Csillik B
Exp Brain Res. 1976 Aug 27;26(1):73-87. doi: 10.1007/BF00235250.
Disappearance of fluorid-resistant acid phosphatase activity from the ipsilateral Rolando substance after transection of the peripheral nerve, is shown to be due to the cessation of enzyme supply from dorsal root ganglion cells to their central terminals. This is accompanied by (or ensues in consequence of) a fine structural derangement of these terminals ("degenerative atrophy"). Fine structural alterations of axon terminals undergoing degenerative atrophy, though similar to some extent to those seen during early phases of a Wallerian degeneration, are markedly different. Also myelinated nerve fibers, both in the dorsal horn and in dorsal columns, are affected by degenerative atrophy. This important, new trophical feature of sensory ganglion cells suggests a delicate metabolic balance between peripheral and central axonal branches of bipolar (pseudounipolar) cells. Degenerative atrophy raises serious implications in evaluating hodological experiments based upon Wallerian degeneration and offers new perspectives for theoretical and clinical neurology.
切断周围神经后,同侧罗兰多氏区抗氟酸性磷酸酶活性消失,这表明是由于背根神经节细胞向其中枢终末的酶供应停止所致。这伴随着(或因之而产生)这些终末的细微结构紊乱(“变性萎缩”)。经历变性萎缩的轴突终末的细微结构改变,尽管在一定程度上与华勒氏变性早期所见相似,但明显不同。此外,背角和背柱中的有髓神经纤维也受到变性萎缩的影响。感觉神经节细胞这一重要的新营养特征提示双极(假单极)细胞的外周和中枢轴突分支之间存在微妙的代谢平衡。变性萎缩在评估基于华勒氏变性的神经传导径路实验时引发了严重问题,并为理论和临床神经病学提供了新的视角。