Neurotrauma is among main causes of human disability and death. We studied effects of axotomy on ultrastructure and neuronal activity of a simple model object – an isolated crayfish stretch receptor that consists of single mechanoreceptor neurons (MRN) enwrapped by multilayer glial envelope. After isolation, MRN regularly fired until spontaneous activity cessation. Axotomy did not change significantly MRN spike amplitude and firing rate. However, the duration of neuron activity from MRN isolation to its spontaneous cessation decreased in axotomized MRN relative to intact neuron. [Ca²⁺] in MRN axon and soma increased 3–10 min after axotomy. Ca²⁺ entry through ion channels in the axolemma accelerated axotomy-stimulated firing cessation. MRN incubation with Ca²⁺ionophore ionomycin accelerated MRN inactivation, whereas Ca²⁺-channel blocker Cd²⁺ prolonged firing. Activity duration of either intact, or axotomized MRN did not change in the presence of ryanodine or dantrolene, inhibitors of ryanodin-sensitive Ca²⁺ channels in endoplasmic reticulum. Thapsigargin, inhibitor of endoplasmic reticulum Ca²⁺-ATPase, or its activator ochratoxin were ineffective. Ultrastructural study showed that the defect in the axon transected by thin scissors is sealed by fused axolemma, glial and collagen layers. Only the 30–50 μm long segment completely lost microtubules and contained swelled mitochondria. The microtubular bundle remained undamaged at 300 μm away from the axotomy site. However, mitochondria within the 200–300 μm segment were strongly condensed and lost matrix and cristae. Glial and collagen layers exhibited greater damage. Swelling and edema of glial layers, collagen disorganization and rupture occurred within this segment. Thus, axotomy stronger damages glia/collagen envelope, axonal microtubules and mitochondria.

神经创伤是人类残疾和死亡的主要原因之一。我们研究了轴突切开术对简单模型对象的超微结构和神经元活动的影响 - 一种孤立的小龙虾拉伸受体，由多层神经胶质包膜包裹的单个机械感受器神经元 (MRN) 组成。隔离后，MRN 会定期发射，直到自发活动停止。轴突切开术没有显着改变 MRN 尖峰振幅和放电率。然而，相对于完整的神经元，轴突切断的 MRN 从 MRN 分离到其自发停止的神经元活动的持续时间减少。MRN 轴突和体细胞中的[Ca ²⁺ ] 在轴突切断后 3-10 分钟增加。Ca ²⁺通过轴突中的离子通道进入加速了轴突切开刺激的放电停止。MRN 与 Ca ²⁺孵育离子载体离子霉素加速 MRN 失活，而 Ca ²⁺通道阻滞剂 Cd ²⁺延长放电。在兰尼定或丹曲林（内质网中兰诺定敏感的 Ca ²⁺通道的抑制剂）存在的情况下，完整或轴突切断的 MRN 的活性持续时间没有变化。毒胡萝卜素，内质网 Ca ²⁺抑制剂-ATPase 或其激活剂赭曲霉毒素无效。超微结构研究表明，被薄剪刀横断的轴突缺损被融合的轴突、神经胶质和胶原层密封。只有 30-50 μm 长的片段完全失去了微管并含有膨胀的线粒体。微管束在离轴突切断部位 300 μm 处保持完好。然而，200-300 μm 段内的线粒体强烈浓缩并丢失基质和嵴。神经胶质和胶原层表现出更大的损伤。该节段内发生胶质层肿胀水肿、胶原解体和破裂。因此，轴突切断术更能破坏神经胶质/胶原包膜、轴突微管和线粒体。