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冷损伤中的神经元完整性和星形胶质细胞反应:一项免疫组织化学研究。

Neuronal integrity and astrocytic reaction in cold injury: an immunohistochemical investigation.

作者信息

Maeda M, Akai F, Yanagihara T

机构信息

Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

Acta Neuropathol. 1997 Aug;94(2):116-23. doi: 10.1007/s004010050682.

DOI:10.1007/s004010050682
PMID:9255385
Abstract

The relationship between extravasation of serum albumin and damage to the neuronal elements as well as the astrocytic reaction was investigated following cold injury, using immunohistochemistry for albumin, microtubule-associated protein I and II (MAPs) and glial fibrillary acidic protein (GFAP). After 30 min, spreading of albumin to the neuropil and uptake into nerve cell bodies and dendrites were clearly observed in the area surrounding the cold lesion. Extravasation of albumin was maximal at 24 h and extended to the ipsilateral hippocampus and thalamus as well as to the paramedian part of the contralateral cerebral hemisphere. Uptake of albumin was seen in neurons with and without loss or reduction of the reaction for MAPs, but the former was confined to the area surrounding the cold lesion. When extravasated albumin receded from the neuropil, the positive reaction for albumin also disappeared from the neuronal elements and those neurons recovered immunoreactivity for MAPs. Astrocytes immunopositive for albumin were observed at 24 h in the white matter, and reactive astrocytes became notable even in the gray matter surrounding the cold lesion. Although reactive astrocytes persisted even after resolution of cerebral edema, immunopositivity for albumin disappeared from astrocytes soon after the disappearance of the reaction from the neuropil. As to the mechanism, rapid endo- and exocytosis may take place in response to the amount of edema fluid in the surrounding extracellular space, where albumin may be eliminated through the transvascular route and/or via the cerebrospinal fluid space.

摘要

采用白蛋白、微管相关蛋白I和II(MAPs)以及胶质纤维酸性蛋白(GFAP)的免疫组织化学方法,研究了冷损伤后血清白蛋白外渗与神经元损伤及星形胶质细胞反应之间的关系。30分钟后,在冷损伤周围区域可清晰观察到白蛋白扩散至神经毡,并被神经细胞体和树突摄取。白蛋白外渗在24小时时达到最大值,并扩展至同侧海马体、丘脑以及对侧大脑半球的旁正中部分。在有或没有MAPs反应丧失或减弱的神经元中均可见白蛋白摄取,但前者局限于冷损伤周围区域。当外渗的白蛋白从神经毡消退时,神经元成分中白蛋白的阳性反应也消失,这些神经元恢复了对MAPs的免疫反应性。在24小时时,在白质中观察到对白蛋白免疫阳性的星形胶质细胞,甚至在冷损伤周围的灰质中反应性星形胶质细胞也变得明显。尽管即使在脑水肿消退后反应性星形胶质细胞仍持续存在,但在神经毡反应消失后不久,星形胶质细胞对白蛋白的免疫阳性就消失了。至于其机制,可能会根据周围细胞外空间中水肿液的量发生快速的内吞和外排作用,白蛋白可能通过跨血管途径和/或通过脑脊液空间被清除。

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