Auer R, Kalimo H, Olsson Y, Wieloch T
Acta Neuropathol. 1985;67(3-4):279-88. doi: 10.1007/BF00687813.
A detailed light- and electron-microscopic study of the damage to the rat dentate gyrus in hypoglycemia was undertaken, in view of the previously advanced hypothesis that hypoglycemic nerve cell injury is mediated by a released neurotoxin. The distribution of neuronal necrosis showed a relationship to the subarachnoid cisterns. Electron microscopy of the dentate granule cells and their apical dendrites revealed dendrosomal, axon-sparing neuronal pathology. Dentate granule cells were affected first in the dendrites in the outer layer of the stratum moleculare, sparing axons of passage and terminal boutons. Subsequently, the neuronal perikarya were affected, and Wallerian degeneration of axons followed. Cell membrane abnormalities preceded the appearance of mitochondrial flocculent densities and degradation of the cytoskeleton, and are suggested to be early lethal changes. The observed early dendrotoxic changes, and the dendrosomal, axon-sparing nature of the lesion implicate an excitotoxin-mediated neuronal necrosis in hypoglycemia.
鉴于之前提出的低血糖神经细胞损伤由释放的神经毒素介导这一假说，对低血糖状态下大鼠齿状回损伤进行了详细的光学和电子显微镜研究。神经元坏死的分布与蛛网膜下池有关。齿状颗粒细胞及其顶端树突的电子显微镜检查显示出树突体、轴突保留的神经元病理学特征。齿状颗粒细胞首先在分子层外层的树突中受到影响，轴突束和终末钮未受影响。随后，神经元胞体受到影响，接着轴突发生华勒氏变性。细胞膜异常先于线粒体絮状密度的出现和细胞骨架的降解，提示这是早期致死性变化。观察到的早期树突毒性变化以及病变的树突体、轴突保留性质表明低血糖时存在兴奋性毒素介导的神经元坏死。
