Happel R D, Banik N L, Balentine J D, Hogan E L
Neurosci Lett. 1984 Aug 31;49(3):279-83. doi: 10.1016/0304-3940(84)90302-1.
CaCl2-induced myelopathy was produced in rats by the application of a solution of CaCl2 to exposed leptomeninges of lumbosacral spinal cord. Equal lengths of remote cervical and lumbar cord were removed at intervals following Ca2+ application. The total Ca2+ in tissue from lumbar cord was significantly elevated over autologous cervical cord and homologous lumber controls after after 2 h. The maximum Ca2+ increase in lumbar cord was 3.9-fold that of homogolous control and was reached by 8 h post Ca2+ application. The time course for the elevation of Ca2+ as measured by atomic absorption spectrophotometry, resembles that found in spinal cord following direct physical trauma. These findings as well as similar changes in morphology and neural proteins from previous studies suggest that Ca2+ is involved in and may potentiate the degeneration of axons and myelin via Ca2+-activated neutral proteinases.
通过将氯化钙溶液应用于大鼠腰骶部脊髓暴露的软脑膜来诱导产生氯化钙诱导的脊髓病。在施加钙离子后，每隔一段时间切除相等长度的远端颈髓和腰髓。钙离子施加2小时后，腰髓组织中的总钙离子含量相对于自体颈髓和同源腰髓对照显著升高。腰髓中钙离子的最大增加量是同源对照的3.9倍，在钙离子施加后8小时达到。通过原子吸收分光光度法测量的钙离子升高的时间进程，类似于直接物理创伤后脊髓中发现的情况。这些发现以及先前研究中形态学和神经蛋白的类似变化表明，钙离子通过钙激活的中性蛋白酶参与并可能增强轴突和髓鞘的退化。
