Ultrastructural analysis of the progression of neurodegeneration in the septum following fimbria-fornix transection
Ultrastructural analysis of the progression of neurodegeneration in the septum following fimbria-fornix transection
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DOI：
10.1016/s0306-4522(98)00136-5
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发表时间：
1998-10-01
期刊：
影响因子：
3.3
通讯作者：
Martin, LJ
中科院分区：
文献类型：
--
作者：
Ginsberg, SD;Martin, LJ
穹窿-海马伞横断范式已被用作内侧隔核内逆行神经变性和外侧隔核内轴突终末顺行变性的模型。由于神经元的维持和存活可能取决于传出和传入的完整性，在成年大鼠单侧穹窿海马伞切断后3、7、14、30天和6个月，对内侧隔核和背外侧隔核中神经元的超微结构进行了分析。在穹窿海马伞横断同侧的两个核中均发生轴突和体树突室的变性。退化的轴突和终端存在3天后消散，虽然退化的轴树突和轴体终端仍然检测到在14-30天postlesion。两个隔核中的树体改变表现为细胞器的重新分布，分散和损失的粗面内质网，膜结合的空泡池和膜状包涵体的形成，细胞质基质的损失，和分散的染色质在整个核质基质。这些变化发生在没有明显的超微结构损伤线粒体和浓缩的细胞核。内侧和背外侧隔核的树突病理在损伤后14-30天最突出，但神经纤维在损伤后6个月恢复到控制外观。与此相反，细胞质稀疏和空泡化的神经元胞体是持久的内侧隔核和背外侧隔nucleus.We的结论是，从海马断开后，超微结构异常发生在内侧和外侧隔核的神经元。这些变化的特征和时间过程在两个核团中是相似的。神经纤毛变性是短暂的，相反，神经元细胞体损伤是持久的，形态学上与长期神经元萎缩一致。(C)1998年IBRO。出版社：Elsevier Science Ltd
The fimbria-fornix transection paradigm has been used as a model of retrograde neurodegeneration within the medial septal nucleus and anterograde degeneration of axon terminals within the lateral septal nucleus. Because the maintenance and survival of neurons may depend on the integrity of both efferents and afferents, the ultrastructure of neurons in the medial septal nucleus and dorsolateral septal nucleus was analysed at three, seven, 14, 30 days, and six months following unilateral transection of the fimbria-fornix in adult rats. Degeneration of axonal and somatodendritic compartments occurred in both nuclei on the side ipsilateral to fimbria-fornix transection. Degeneration of axons and terminals was present by three days and dissipated thereafter, although degenerating axodendritic and axosomatic terminals were still detected at 14-30 days postlesion. Dendrosomal alterations in both septal nuclei manifested as redistribution of organelles, dispersion and loss of rough endoplasmic reticulum, formation of membrane-bound vacuolar cisternae and membranous inclusions, loss of cytoplasmic matrix, and dispersion of chromatin throughout the nucleoplasmic matrix. These changes occurred in the absence of apparent ultrastructural damage to mitochondria and condensation of the nucleus. Dendritic pathology in both the medial and dorsolateral septal nuclei was most prominent at 14-30 days postlesion, but the neuropil recovered to control appearance by six months postlesion. In contrast, the cytoplasmic rarefaction and vacuolation of neuronal cell bodies were persistent in both the medial septal nucleus and the dorsolateral septal nucleus.We conclude that, following disconnection from the hippocampus, ultrastructural abnormalities occur within neurons in both the medial and lateral septal nuclei. The characteristics and time-course for these changes are similar in both nuclei. The neuropilar degeneration was transient, in contrast to the neuronal cell body injury which was persistent and was morphologically consistent with long-term neuronal atrophy. (C) 1998 IBRO. Published by Elsevier Science Ltd.