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首页> 外文期刊>Neurological Research: An Interdisciplinary Quarterly Journal >The expression and distribution of seizure-related and synaptic proteins in the insular cortex of rats genetically prone to audiogenic seizures
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The expression and distribution of seizure-related and synaptic proteins in the insular cortex of rats genetically prone to audiogenic seizures

机译:遗传易发音源性癫痫的大鼠小岛皮层中癫痫相关蛋白和突触蛋白的表达和分布

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摘要

It is known that perirhinal/insular cortices participate in the transmission of sensory stimuli to the motor cortex, thus coordinating motor activity during seizures. In the present study we analysed seizure-related proteins, such as GABA, glutamate, ERK1/2 and the synaptic proteins in the insular cortex of Krushinsky-Molodkina (KM) rats genetically prone to audiogenic seizures (AGS). We compared seizure-naive and seizure-experienced KM rats with control Wistar rats in order to distinguish whether seizure-related protein changes are associated with seizure event or representing an inhered pathological abnormality that determines predisposition to AGS. Our data demonstrated an increased level of vesicular glutamate transporter VGLUT2 in naive and seizure-experienced KM rats, while glutamic acid decarboxylases GAD65 and GAD67 levels were unchanged. Evaluation of the synaptic proteins showed a decrease in SNAP-25 and upregulation of synapsin I phosphorylation in both groups of KM rats in comparison to Wistar rats. However, when phosphorylation level of ERK1/2 in naive KM rats was significantly increased, several episodes of AGS diminished ERK1/2 activity. Obtained data indicate that changes in ERK1/2 phosphorylation status and glutamate release controlling synaptic proteins in the insular cortex of KM rats could contribute to the AGS susceptibility.
机译:众所周知,周围/皮层皮质参与感觉刺激向运动皮层的传递,从而在癫痫发作期间协调运动活动。在本研究中,我们分析了遗传上倾向于音源性癫痫发作(AGS)的Krushinsky-Molodkina(KM)大鼠小岛皮层中与癫痫发作相关的蛋白,例如GABA,谷氨酸,ERK1 / 2和突触蛋白。我们将未发作和未发作的KM大鼠与对照Wistar大鼠进行了比较,以区分癫痫相关的蛋白质变化是否与癫痫发作有关或代表固有的病理异常,从而决定了AGS的易感性。我们的数据表明,在幼稚和癫痫发作的KM大鼠中,水泡谷氨酸转运蛋白VGLUT2的水平升高,而谷氨酸脱羧酶GAD65和GAD67的水平未改变。与Wistar大鼠相比,两组KM大鼠中突触蛋白的评估显示SNAP-25降低和突触素I磷酸化上调。但是,当幼稚的KM大鼠中ERK1 / 2的磷酸化水平显着增加时,几次AGS发作都会降低ERK1 / 2的活性。获得的数据表明,KM大鼠小岛皮层中ERK1 / 2磷酸化状态和谷氨酸释放控制突触蛋白的变化可能有助于AGS敏感性。

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