Roederer E, Cohen M J
J Neurosci. 1983 Sep;3(9):1848-59. doi: 10.1523/JNEUROSCI.03-09-01848.1983.
The cell body of the medial giant interneuron (MGI) in the cricket normally does not spike in response to injected depolarizing currents. When axotomized 1 mm or more from the cell body (distant axotomy), the membrane properties of the soma remain unchanged. However, after axotomy close to the cell body (200 to 500 micron), the soma membrane becomes capable of generating action potentials by 6 hr after lesion. These regenerative spikes are 1 to 1.5 msec in duration and may reach 100 mV in peak amplitude. Ion substitutions indicate that these action potentials are primarily sodium dependent. A calcium-dependent component of soma membrane excitability that is normally present appears to be unaffected by axotomy. By 48 hr, the close axotomized MGI somata have lost the ability to generate action potentials and the membrane electrical properties return to normal. By 2 days after axotomy close to the soma, large, membrane-bound, electron-lucent vacuoles appear in the cytoplasm of the MGI cell body. Such vacuoles then disappear from axotomized MGI somata by 10 days. In addition, numerous arrays of densely packed, darkly staining microtubules are observed in the cell body, especially concentrated near the initial neurite. Neither of these specialized structures is observed in control, intact MGI somata. We propose that close axotomy disrupts the mechanisms which regulate the stability of the fully mature, differentiated neuron. The characteristic morphological and physiological stability of the MGI is lost: the dendritic arborization has been shown previously to be altered by extensive new outgrowth (Roederer, E., and M. J. Cohen (1983) J. Neurosci. 3: 1835-1847); there is a transient increase in soma membrane excitability, and new cytoplasmic organelles are induced.
蟋蟀体内内侧巨型中间神经元（MGI）的细胞体通常不会因注入去极化电流而产生动作电位。当从细胞体切断1毫米或更远距离的轴突（远距离轴突切断）时，胞体的膜特性保持不变。然而，在靠近细胞体（200至500微米）进行轴突切断后，损伤后6小时胞体膜就能够产生动作电位。这些再生动作电位的持续时间为1至1.5毫秒，峰值幅度可能达到100毫伏。离子置换表明这些动作电位主要依赖于钠离子。通常存在的胞体膜兴奋性的钙依赖成分似乎不受轴突切断的影响。到48小时时，靠近轴突切断的MGI胞体已经失去了产生动作电位的能力，膜电特性恢复正常。在靠近胞体进行轴突切断2天后，MGI细胞体的细胞质中出现大的、膜结合的、电子透明的空泡。到10天时，这些空泡从轴突切断的MGI胞体中消失。此外，在细胞体中观察到大量密集排列、深色染色的微管阵列，尤其集中在初始神经突附近。在对照的完整MGI胞体中未观察到这些特殊结构中的任何一种。我们提出，靠近轴突切断会破坏调节完全成熟、分化神经元稳定性的机制。MGI的特征性形态和生理稳定性丧失：先前已表明树突分支会因广泛的新生长而改变（罗德勒，E.，和M. J. 科恩（1983年）《神经科学杂志》3：1835 - 1847）；胞体膜兴奋性短暂增加，并且诱导产生新的细胞质细胞器。
