Arvidsson J
J Comp Neurol. 1986 Jul 15;249(3):392-403. doi: 10.1002/cne.902490306.
Previous studies have shown that transection of peripheral branches of primary sensory neurons leads to light microscopical degeneration argyrophilia and ultrastructural changes in the central termination areas of these neurons. This type of degeneration has been termed transganglionic degeneration (TGD). In the present experiments TGD has been studied specifically in neurons innervating the rat vibrissae at the light and electron microscopic levels. Light microscopically, small amounts of degeneration argyrophilia are observed in the magnocellular zone of the trigeminal subnucleus caudalis at 8-14 days survival. At longer survival times there are substantial amounts of degeneration in this area. At the ultrastructural level the first signs of TGD are observed at 6 days survival, when some terminals show a small increase in electron density, loss of synaptic vesicles, and mitochondrial disintegration. Terminals showing a more advanced increase in electron density become common at 8 days survival, but few of them are still left at 14 days survival. Neurofilamentous terminals appear in small numbers 8-14 days postoperatively. Various forms of degeneration in myelinated axons are observed from 8 days survival and are common also at 80 days survival. Electron-dense axons are rather unfrequent, but more or less disrupted myelin sheaths containing disintegrated axoplasmic remnants and empty areas are common as well as extremely expanded myelin sheaths. Glial cells containing axonal and myelin debris are seen from 8 days survival and become a more common finding at longer survivals. A most striking finding 8-10 days postoperatively is a complex relationship between glial cells and less darkened terminals, indicating phagocytosis before reaching an entirely darkened state. The findings clearly show that peripheral nerve transection leads to severe central alterations in a population of mechanoreceptor neurons innervating the vibrissae of the adult rat.
先前的研究表明,切断初级感觉神经元的外周分支会导致这些神经元的中枢终末区域出现光镜下的变性嗜银性和超微结构变化。这种类型的变性被称为跨节变性(TGD)。在本实验中,已在光镜和电镜水平上专门研究了支配大鼠触须的神经元中的TGD。光镜下,在存活8 - 14天时,三叉神经尾侧亚核的大细胞区观察到少量变性嗜银性。在更长的存活时间里,该区域出现大量变性。在超微结构水平上,TGD的最初迹象在存活6天时被观察到,此时一些终末显示电子密度略有增加、突触小泡丢失和线粒体解体。在存活8天时,显示电子密度进一步增加的终末变得常见,但在存活14天时,其中很少有留存。术后8 - 14天出现少量神经丝终末。从存活8天起观察到有髓轴突的各种变性形式,在存活80天时也很常见。电子致密的轴突相当少见,但含有解体轴浆残余物和空洞区域的或多或少被破坏的髓鞘以及极度扩张的髓鞘也很常见。从存活8天起可见含有轴突和髓鞘碎片的胶质细胞,在更长的存活时间里成为更常见的发现。术后8 - 10天最显著的发现是胶质细胞与颜色较浅的终末之间的复杂关系,表明在达到完全变黑状态之前存在吞噬作用。这些发现清楚地表明,外周神经切断会导致成年大鼠触须的一群机械感受器神经元发生严重的中枢改变。