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微管相关蛋白 2 作为脊髓损伤后树突损伤的敏感标志物:在大鼠中的免疫组织化学研究。

Microtubule-associated protein 2 as a sensitive marker for dendrite lesions after spinal cord trauma: an immunohistochemical study in the rat.

机构信息

Laboratory of Neuropathology, University Hospital, S-751 85 Uppsala, Sweden.

出版信息

Restor Neurol Neurosci. 1995 Jan 1;8(4):189-97. doi: 10.3233/RNN-1995-8404.

DOI:10.3233/RNN-1995-8404
PMID:21551824
Abstract

We evaluated, by irnmunohistochemistry, the changes of microtubule-associated protein 2 (MAP2) of rat spinal cord following compression injury of mild, moderate and severe degrees at the Th8-9 level. The spinal cord of normal rats and animals subjected to laminectomy only, presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following moderate and severe compression resulting in reversible paraparesis or irreversible paraplegia, respectively, the compressed segment showed loss of MAP2 immunoreactivity in dendrites and nerve cell bodies already 4 h after injury. This phenomenon remained throughout the experimental period of 9 days. Our findings indicate that there is a rapid and long-lasting reduction of MAP2 in nerve cell bodies and dendrites of the compressed segment and that this alteration is related to the degree of the impact to the cord. The reduction of MAP2 may well have functional implications by interfering with neurotransmission. MAP2 immuno-staining is an excellent way of studying dendritic changes in spinal cord trauma and can be used in future experiments designed to investigate the influence of various therapeutic measures on secondary lesions after trauma.

摘要

我们通过免疫组织化学方法评价了大鼠 Th8-9 水平轻度、中度和重度压迫损伤后脊髓微管相关蛋白 2(MAP2)的变化。正常大鼠和仅接受椎板切除术的动物的脊髓,在神经细胞体和树突中呈现 MAP2 免疫反应,但在轴突和其他结构中没有。中度和重度压迫分别导致可逆性截瘫或不可逆性截瘫后,受压段在损伤后 4 小时即出现树突和神经细胞体中 MAP2 免疫反应的丧失。这种现象在整个 9 天的实验期间一直存在。我们的研究结果表明,受压段的神经细胞体和树突中的 MAP2 迅速且持续减少,这种改变与脊髓的损伤程度有关。MAP2 的减少可能通过干扰神经递质传递而具有功能意义。MAP2 免疫染色是研究脊髓创伤中树突变化的一种极好方法,可用于未来的实验,旨在研究各种治疗措施对创伤后继发性损伤的影响。

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引用本文的文献

1
Expression of ubiquitin-like immunoreactivity in axons after compression trauma to rat spinal cord.
Acta Neuropathol. 1996;91(2):155-60. doi: 10.1007/s004010050407.