Pellegrino R G, Politis M J, Ritchie J M, Spencer P S
J Neurocytol. 1986 Feb;15(1):17-28. doi: 10.1007/BF02057901.
Severance of a peripheral nerve leads to a characteristic series of events in the distal stump, including the dissolution of axons and myelin and the proliferation of Schwann cells within their basal lamina. This study examines the relationship between the spatial-temporal pattern of the induction of the Schwann cell S phase, loss of the structural and functional properties of axolemma, and the clearance of myelin debris in the cat tibial nerve. Nerve transection stimulated a monophasic increase in [3H]thymidine incorporation that peaked at 4 days post-transection throughout an 80-mm length of distal stump. Light microscope autoradiography revealed prominent incorporation into Schwann cells of myelinated fibres. Treatment of distal stumps with mitomycin C at the time of nerve transection greatly retarded thymidine incorporation and clearance of myelin debris, but not the time course of axonal degeneration, decline in the synthesis of the major myelin glycoprotein, P0, or the onset of ovoid formation. Nerve transection also greatly reduced the specific uptake of [3H]saxitoxin (STX), a ligand which binds to voltage-sensitive sodium channels. Binding in the distal stump fell precipitously to 20% of the normal at 4 days post-transection, concurrent with the peak of thymidine incorporation. This low level of binding was maintained for periods of up to 70 days, demonstrating that some STX binds to structures other than axons in denervated distal stumps. Prior treatment with mitomycin C delayed the loss of specific STX binding. In conclusion, these studies suggest that: Schwann cell DNA replication and/or mitosis regulates other events during Wallerian degeneration, including myelin degeneration, catabolism of P0 and the clearance of sodium channels from nodal axolemma; the decline in P0 synthesis and/or shift to synthesis of less extensively processed P0 is independent of the induction of Schwann cell S phase; and Schwann cells enveloping myelinated axons enter S phase within a 24-h period throughout the entire 80-mm length of distal stump.
外周神经切断会导致远端残端发生一系列特征性事件,包括轴突和髓鞘的溶解以及施万细胞在其基膜内的增殖。本研究探讨了猫胫神经中施万细胞S期诱导的时空模式、轴膜结构和功能特性的丧失以及髓鞘碎片清除之间的关系。神经横断刺激了[3H]胸腺嘧啶核苷掺入的单相增加,在横断后4天达到峰值,贯穿80毫米长的远端残端。光学显微镜放射自显影显示有髓纤维的施万细胞中有明显的掺入。在神经横断时用丝裂霉素C处理远端残端极大地延迟了胸腺嘧啶核苷掺入和髓鞘碎片的清除,但不影响轴突退变的时间进程、主要髓鞘糖蛋白P0合成的下降或卵圆体形成的开始。神经横断还大大降低了[3H]石房蛤毒素(STX)的特异性摄取,STX是一种与电压敏感钠通道结合的配体。横断后4天,远端残端的结合急剧下降至正常水平的20%,与胸腺嘧啶核苷掺入的峰值同时出现。这种低水平的结合持续长达70天,表明在去神经的远端残端中,一些STX与轴突以外的结构结合。丝裂霉素C预处理延迟了特异性STX结合的丧失。总之,这些研究表明:施万细胞DNA复制和/或有丝分裂调节沃勒变性期间的其他事件,包括髓鞘变性、P0的分解代谢以及从结间轴膜清除钠通道;P0合成的下降和/或向加工程度较低的P0合成的转变与施万细胞S期的诱导无关;包裹有髓轴突的施万细胞在整个80毫米长的远端残端内的24小时内进入S期。