Rosenberg L J, Emery D G, Lucas J H
Department of Neuroscience, Georgetown University, Washington, DC, USA.
J Neuropathol Exp Neurol. 2001 Jan;60(1):33-48. doi: 10.1093/jnen/60.1.33.
An in vitro investigation was undertaken to study the roles of Na+ and Cl- in mammalian spinal cord (SC) neuron deterioration and death after injury involving physical disruption of the plasma membrane. Individual SC neurons in monolayer cultures were subjected to UV laser microbeam transection of a primary dendrite. Neurons lesioned in modified ionic environments (MIEs) where 50%-75% of the NaCl was replaced with sucrose had higher survival (65%-75%) than neurons lesioned in medium with normal (125 mM) NaCl (28%; p < 0.001). Subsequent experiments found a comparable increase in lesioned neuron survival in MIEs in which only Na+ was replaced with specific ionic substitutes; however, replacement of Cl- was not protective. Electron microscope examinations of neurons fixed <16 min after lesioning showed a dramatic decrease in vesiculation of the smooth endoplasmic reticulum and Golgi apparatus in the low NaCl or low Na+ MIEs. It is hypothesized that Na+ entry after membrane disruption may stimulate elevation of [Ca+2]i leading to ultrastructural disruption and death of injured neurons. The results of these studies suggest that a low NaCl MIE may be useful as an irrigant to limit damage spread and cell death within CNS tissues during surgery or after trauma.
进行了一项体外研究，以探讨Na⁺和Cl⁻在哺乳动物脊髓（SC）神经元因涉及质膜物理破坏的损伤后退化和死亡中的作用。单层培养中的单个SC神经元接受初级树突的紫外激光微束横切。在50%-75%的NaCl被蔗糖替代的改良离子环境（MIE）中受损的神经元，其存活率（65%-75%）高于在含有正常（125 mM）NaCl的培养基中受损的神经元（28%；p<0.001）。随后的实验发现，在仅用特定离子替代物替代Na⁺的MIE中，受损神经元的存活率有类似的增加；然而，替代Cl⁻并无保护作用。对损伤后<16分钟固定的神经元进行电子显微镜检查发现，在低NaCl或低Na⁺的MIE中，滑面内质网和高尔基体的囊泡化显著减少。据推测，膜破坏后Na⁺的进入可能会刺激细胞内Ca²⁺浓度升高，导致受损神经元的超微结构破坏和死亡。这些研究结果表明，低NaCl的MIE可作为一种冲洗剂，在手术或创伤后限制中枢神经系统组织内的损伤扩散和细胞死亡。
