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出生后发育过程中易发生听源性癫痫的大鼠下丘中ERK1/2激酶的分析

Analysis of ERK1/2 kinases in the inferior colliculus of rats genetically prone to audiogenic seizures during postnatal development.

作者信息

Chernigovskaya E V, Lebedenko O O, Nidenfyur A V, Nikitina L S, Glazova M V

机构信息

Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, 194223, Russia.

出版信息

Dokl Biochem Biophys. 2017 Sep;476(1):296-298. doi: 10.1134/S1607672917050015. Epub 2017 Nov 4.

DOI:10.1134/S1607672917050015
PMID:29101749
Abstract

The activity of ERK1/2 kinases in the quadrigemina inferior colliculus of Krushinsky-Molodkina rats of different age, which are characterized by an increased seizure readiness compared to Wistar rats, was analyzed. An increased (probably genetically determined) activity of these enzymes during the development of epileptiform activity in ontogeny was found, which may be the cause of abnormalities in the neurotransmitter system functioning.

摘要

对不同年龄的克鲁申斯基-莫洛迪纳大鼠下丘臂中ERK1/2激酶的活性进行了分析,与Wistar大鼠相比,这些大鼠的癫痫发作易感性增加。发现在个体发育过程中癫痫样活动发展期间这些酶的活性增加(可能是基因决定的),这可能是神经递质系统功能异常的原因。

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本文引用的文献

1
The expression and distribution of seizure-related and synaptic proteins in the insular cortex of rats genetically prone to audiogenic seizures.在遗传性易患听源性癫痫大鼠的岛叶皮质中癫痫相关蛋白和突触蛋白的表达及分布
Neurol Res. 2015;37(12):1108-17. doi: 10.1080/01616412.2015.1114288.
2
[COMPARATIVE STUDY OF NIGROSTRIATAL SYSTEMS IN WISTAR RATS AND RATS PRONE TO SEIZURES].[Wistar大鼠与癫痫易感性大鼠黑质纹状体系统的比较研究]
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Inhibition of ERK1/2 signaling prevents epileptiform behavior in rats prone to audiogenic seizures.
ERK1/2 信号通路的抑制可预防易发生听觉性癫痫发作大鼠的癫痫样行为。
J Neurochem. 2015 Jan;132(2):218-29. doi: 10.1111/jnc.12982. Epub 2014 Nov 14.
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Resilience to audiogenic seizures is associated with p-ERK1/2 dephosphorylation in the subiculum of Fmr1 knockout mice.对听觉惊厥的抵抗力与 Fmr1 敲除小鼠下托区 p-ERK1/2 去磷酸化有关。
Front Cell Neurosci. 2013 Apr 25;7:46. doi: 10.3389/fncel.2013.00046. eCollection 2013.
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Activation of ERK by spontaneous seizures in neural progenitors of the dentate gyrus in a mouse model of epilepsy.癫痫小鼠模型中海马齿状回神经祖细胞自发痫性放电激活 ERK。
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Dynamic seizure-related changes in extracellular signal-regulated kinase activation in a mouse model of temporal lobe epilepsy.颞叶癫痫小鼠模型中与发作相关的细胞外信号调节激酶激活的动态变化
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ERK activation causes epilepsy by stimulating NMDA receptor activity.细胞外信号调节激酶(ERK)激活通过刺激N-甲基-D-天冬氨酸(NMDA)受体活性导致癫痫。
EMBO J. 2007 Nov 28;26(23):4891-901. doi: 10.1038/sj.emboj.7601911. Epub 2007 Nov 1.
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Extracellularly regulated kinases 1/2 (p44/42 mitogen-activated protein kinases) phosphorylate synapsin I and regulate insulin secretion in the MIN6 beta-cell line and islets of Langerhans.细胞外调节激酶1/2(p44/42丝裂原活化蛋白激酶)使突触结合蛋白I磷酸化,并调节MIN6β细胞系和胰岛中的胰岛素分泌。
Endocrinology. 2005 Feb;146(2):643-54. doi: 10.1210/en.2004-0841. Epub 2004 Oct 21.
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