组织蛋白酶抑制剂处理载脂蛋白e缺陷小鼠海马锥体神经元超微结构分析。

Sofia Díaz-Cintra, Alex Yong, Azucena Aguilar, Xiaoning Bi, Gary Lynch, Charles E Ribak
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引用次数: 13

摘要

将载脂蛋白E (apoE)缺失小鼠的培养海马切片暴露于组织蛋白酶B和L抑制剂中,然后进行锥体细胞体神经元特征的超微结构分析。电镜观察显示,处理后的海马锥体细胞的细胞核比未处理的海马锥体细胞更偏心。此外,囊泡数量的增加与高尔基复合体有关,而微管在近端树突中较少出现。与先前对大鼠的研究一致,处理过的apoe缺陷切片增加了溶酶体和多泡体的数量。最后,细胞体周围的突触数量减少,这一发现与阿尔茨海默病患者大脑中的发现相似。这些结果提供了超微结构数据,表明apoe缺陷脑的部分溶酶体功能障碍迅速诱导了老年人脑的特征。
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Ultrastructural analysis of hippocampal pyramidal neurons from apolipoprotein E-deficient mice treated with a cathepsin inhibitor.

Cultured hippocampal slices prepared from apolipoprotein E (apoE)-deficient mice were exposed to an inhibitor of cathepsins B and L and then processed for an ultrastructural analysis of neuronal features for pyramidal cell bodies. Electron microscopy showed that the nuclei of pyramidal cells from treated hippocampal slices were more eccentrically located than those from untreated slices. In addition, increased numbers of vesicles were associated with the Golgi complex while microtubules were less frequent in the proximal dendrites. Consistent with previous studies in rats, treated apoE-deficient slices had increased numbers of lysosomes and multivesicular bodies. Finally, there were reductions in the number of synapses around the cell body, a finding similar to that found in the brains from Alzheimer's disease patients. These results provide ultrastructural data indicating that partial lysosomal dysfunction in apoE-deficient brains rapidly induces characteristic features of the aged human brain.

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