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杏仁核点燃大鼠海马中的Nogo-A与改良Timm染色

Hippocampal Nogo-A and neo-Timm's staining in amygdala kindling rats.

作者信息

Takeda Yu, Kamida Tohru, Fujiki Minoru, Kobayashi Hidenori

机构信息

Department of Neurosurgery, Oita University Faculty of Medicine, Oita, Japan.

出版信息

Neurol Res. 2007 Mar;29(2):199-203. doi: 10.1179/016164107X188232.

DOI:10.1179/016164107X188232
PMID:17439704
Abstract

PURPOSE

Nogo-A, one of the axon regeneration inhibitors, has been shown to be up-regulated in both the experimental and human temporal lobe epilepsy. However, the role of Nogo-A in mossy fiber sprouting (MFS) relative to epileptogenesis is unknown. This work was designed to examine the relationship of the hippocampal Nogo-A protein expression with MFS during the development of amygdala kindling.

METHODS

Using immunohistochemistry and neo-Timm's histological procedures, we evaluated the distribution and density of Nogo-A and Nogo-66 receptor (Ng-R) expression and MFS in the bilateral hippocampus of amygdala kindling rats.

RESULTS

Nogo-A expression in the ipsilateral hippocampus gradually increased with the development of kindling in the sector CA2-3. In contrast, no increased Nogo-A expression was observed in the contralateral hippocampus as the rats advanced to stage 5 kindled seizures. Furthermore, poorer Nogo-A and Nogo-66 receptor (Ng-R) expression were observed in the dentate granule cells as aberrant MFS occurred.

CONCLUSIONS

In amygdala kindling rats, generalized stage 5 seizures were not associated with increased Nogo-A expression in the contralateral hippocampus supporting the concept that seizures by themselves do not induce Nogo-A expression. Furthermore, in the ipsilateral hippocampus, the expression of Nogo-A relative to MSF suggests that this protein may partially control aberrant synaptic reorganization during epileptogenesis.

摘要

目的

轴突再生抑制因子之一的Nogo-A已被证明在实验性和人类颞叶癫痫中均上调。然而,Nogo-A在苔藓纤维出芽(MFS)中相对于癫痫发生的作用尚不清楚。本研究旨在探讨杏仁核点燃过程中海马Nogo-A蛋白表达与MFS的关系。

方法

采用免疫组织化学和改良的Timm组织学方法,评估杏仁核点燃大鼠双侧海马中Nogo-A和Nogo-66受体(Ng-R)表达的分布和密度以及MFS情况。

结果

随着点燃在CA2-3区的发展,同侧海马中Nogo-A表达逐渐增加。相反,随着大鼠发展到第5期点燃发作,对侧海马中未观察到Nogo-A表达增加。此外,当出现异常MFS时,齿状颗粒细胞中Nogo-A和Nogo-66受体(Ng-R)表达较差。

结论

在杏仁核点燃大鼠中,全身性第5期发作与对侧海马中Nogo-A表达增加无关,支持癫痫发作本身不会诱导Nogo-A表达这一观点。此外,在同侧海马中,Nogo-A相对于MSF的表达表明该蛋白可能在癫痫发生过程中部分控制异常的突触重组。

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