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一种新型自发性癫痫动物模型:周细胞特异性小鼠中的Cdk5基因敲除。

A novel animal model of spontaneous epilepsy: Cdk5 knockout in pericyte-specific mice.

作者信息

Lin Lin, Hu Xiaofei, Hong Weijun, Pan Tengwei, Wang Zhiren, Wang En, Wu Gang

机构信息

Department of Pharmacy, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, Zhejiang, China.

School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang, China.

出版信息

Front Cell Neurosci. 2024 Oct 16;18:1474231. doi: 10.3389/fncel.2024.1474231. eCollection 2024.

DOI:10.3389/fncel.2024.1474231
PMID:39479522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11521856/
Abstract

Changes in neurovascular unit components and their interactions play a crucial role in epileptogenesis and the pathological process of epilepsy. Currently, there is a lack of animal models that can accurately reflect the etiological impact of cerebrovascular lesions on epilepsy. In this study, we constructed cyclin-dependent kinase 5 conditional knockout mice in Cspg4 (pericyte marker)-positive cells using the Cre-LoxP system. The results revealed that this strain of mice exhibited significant seizure behaviors and epileptiform brain waves, loss of hippocampal and amygdala neurons, astrogliosis, decreased pericyte coverage, and reduced AQP4 polar distribution. Herein, we have developed a novel mouse model of spontaneous epilepsy, providing a critical animal model for studying the involvement of neurovascular unit factors in the development and progression of epilepsy.

摘要

神经血管单元成分的变化及其相互作用在癫痫发生和癫痫的病理过程中起着至关重要的作用。目前,缺乏能够准确反映脑血管病变对癫痫病因学影响的动物模型。在本研究中,我们使用Cre-LoxP系统在Cspg4(周细胞标志物)阳性细胞中构建了细胞周期蛋白依赖性激酶5条件性敲除小鼠。结果显示,该品系小鼠表现出明显的癫痫发作行为和癫痫样脑电波,海马和杏仁核神经元丢失,星形胶质细胞增生,周细胞覆盖减少,以及水通道蛋白4极性分布降低。在此,我们开发了一种新型的自发性癫痫小鼠模型,为研究神经血管单元因素在癫痫发生和发展中的作用提供了关键的动物模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a0/11521856/7f0af550cb32/fncel-18-1474231-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a0/11521856/a32c4b066289/fncel-18-1474231-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a0/11521856/7f0af550cb32/fncel-18-1474231-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a0/11521856/a32c4b066289/fncel-18-1474231-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1a0/11521856/7f0af550cb32/fncel-18-1474231-g002.jpg

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本文引用的文献

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The metabolic basis of epilepsy.癫痫的代谢基础。
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Animal Models of Epilepsy: A Phenotype-oriented Review.癫痫的动物模型:一项以表型为导向的综述。
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Breakdown of blood brain barrier as a mechanism of post-traumatic epilepsy.血脑屏障破坏作为创伤后癫痫的机制。
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