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拉伸损伤的中枢神经纤维慢性相轴突和细胞体病变的体视学和超微结构。

Stereology and ultrastructure of chronic phase axonal and cell soma pathology in stretch-injured central nerve fibers.

机构信息

Department of Anatomy, College of Medicine, Veterinary Medicine and Life Sciences, Thomson Building, University of Glasgow, Glasgow, Scotland.

出版信息

J Neurotrauma. 2011 Mar;28(3):383-400. doi: 10.1089/neu.2010.1707.

DOI:10.1089/neu.2010.1707
PMID:21190396
Abstract

Magnetic resonance imaging (MRI) suggests that with survival after human traumatic brain injury (TBI), there is ongoing loss of white and grey matter from the injured brain during the chronic phase. However; direct quantitative experimental evidence in support of this observation is lacking. Using the guinea pig stretch-injury optic nerve model, quantitative evidence by stereology of damage to the optic nerve and retina was sought. Stretch injury was applied to the right optic nerve of 15 adult male guinea pigs. Three animals each at 1, 2, 3, 8, or 12 weeks' survival were killed and prepared for transmission electron microscopy (TEM). The estimated number of intact and injured axons within bins of transverse diameters 0-0.5, 0.51-1.0, 1.01-1.5, 1.51-2.0, 2.01-2.5, and 2.51-3.0 μm in the middle segment of each injured optic nerve and from 5 control animals were compared across all survival time points. The estimated numbers of intact and pyknotic retinal ganglion cells from the same animals were also compared. Loss of myelinated fibers continued throughout the experimental period. The most rapid loss was of the largest fibers; loss of intermediate-sized fibers continued, but the numbers of the smallest fibers increased from 3 weeks onward. There was hypertrophy and proliferation of glial cells within the surrounding neuropil. A relatively low-grade loss of retinal ganglion cells occurred throughout the experiment, with about 60% remaining at 12 weeks' survival. We provide quantitative evidence that after traumatic axonal injury (TAI) there is a continuing loss of nerve fibers and their cell bodies from a CNS tract over a 3-month post-traumatic interval.

摘要

磁共振成像(MRI)表明,在人类创伤性脑损伤(TBI)后存活的情况下,慢性期受伤大脑的白质和灰质仍在持续丢失。然而,目前缺乏支持这一观察结果的直接定量实验证据。本研究使用豚鼠牵拉伤视神经模型,通过体视学寻求视神经和视网膜损伤的定量证据。将牵拉伤施加于 15 只成年雄性豚鼠的右侧视神经。3 只动物在 1、2、3、8 或 12 周存活时处死并准备进行透射电子显微镜(TEM)检查。在受伤视神经中段的每个横向直径 0-0.5、0.51-1.0、1.01-1.5、1.51-2.0、2.01-2.5 和 2.51-3.0μm 的bins 内,估计每个受伤视神经的完整和损伤轴突数量,以及来自 5 只对照动物的数量,在所有存活时间点进行比较。还比较了来自相同动物的完整和固缩视网膜神经节细胞的数量。有髓纤维的丢失在整个实验期间持续发生。丢失最快的是最大纤维;中等大小纤维的丢失继续,但最小纤维的数量从 3 周开始增加。在周围神经胶质中存在神经胶质细胞的肥大和增殖。在整个实验过程中,视网膜神经节细胞发生相对低水平的丢失,在 12 周存活时约有 60%的细胞存活。我们提供了定量证据,表明在创伤性轴索损伤(TAI)后,在创伤后 3 个月的时间内,中枢神经系统(CNS)束中的神经纤维及其细胞体持续丢失。

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