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缝隙连接蛋白/CX3CR1 系统在匹罗卡品诱导的癫痫持续状态后神经元死亡中的作用。

The roles of fractalkine/CX3CR1 system in neuronal death following pilocarpine-induced status epilepticus.

机构信息

Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.

出版信息

J Neuroimmunol. 2011 May;234(1-2):93-102. doi: 10.1016/j.jneuroim.2011.03.005. Epub 2011 Apr 8.

DOI:10.1016/j.jneuroim.2011.03.005
PMID:21481949
Abstract

Although fractalkine is one of chemokines involved in mediation of neuronal/microglial interaction, it is not known whether fractalkine/CX3CR1-mediated pathogenesis occurs in the rat brain following epileptogenic insults. In order to elucidate the roles of the fractalkine/CX3CR1 system in microglial activation and neurodegeneration induced by status epilepticus (SE), we investigated changes in fractalkine/CX3CR1 system within the rat hippocampus following SE. In non-SE induced animals, fractalkine and CX3CR1 immunoreactivity was detected in neurons and microglia, respectively. Following SE, fractalkine immunoreactivity was transiently increased in neurons and astrocytes. CX3CR1 immunoreactivity was also transiently detected in neurons (particularly in CA1 pyramidal cells). Intracerebroventricular infusions of recombinant rat fractalkine aggravated SE-induced neuronal damage, while fractalkine IgG or CX3CR1 IgG infusion alleviated it, compared to saline-infused animals. These findings suggest that fractalkine/CX3CR1 system may play an important role in SE-induced neuronal damages via neuron-microglial interactions.

摘要

尽管趋化因子 fractalkine 是参与神经元/小胶质细胞相互作用的调节因子之一,但尚不清楚 fractalkine/CX3CR1 介导的发病机制是否会在癫痫发作后发生在大鼠大脑中。为了阐明 fractalkine/CX3CR1 系统在癫痫持续状态(SE)诱导的小胶质细胞激活和神经退行性变中的作用,我们研究了 SE 后大鼠海马体中 fractalkine/CX3CR1 系统的变化。在非 SE 诱导的动物中,fractalkine 和 CX3CR1 免疫反应性分别存在于神经元和小胶质细胞中。SE 后,神经元和星形胶质细胞中的 fractalkine 免疫反应性短暂增加。CX3CR1 免疫反应性也在神经元中短暂检测到(特别是在 CA1 锥体神经元中)。与生理盐水输注动物相比,重组大鼠 fractalkine 的脑室内输注加重了 SE 诱导的神经元损伤,而 fractalkine IgG 或 CX3CR1 IgG 的输注则减轻了这种损伤。这些发现表明,fractalkine/CX3CR1 系统可能通过神经元-小胶质细胞相互作用在 SE 诱导的神经元损伤中发挥重要作用。

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