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转基因和药物诱导失神癫痫模型中棘波放电的独特地形模式

Distinct Topographical Patterns of Spike-Wave Discharge in Transgenic and Pharmacologically Induced Absence Seizure Models.

作者信息

Lee Soojung, Hwang Eunjin, Lee Mina, Choi Jee Hyun

机构信息

Department of Oral Physiology, Faculty of Dentistry, Kyung Hee University, Seoul 02447, Korea.

Center for Neuroscience, Korea Institute of Science and Technology, Seoul 02792, Korea.

出版信息

Exp Neurobiol. 2019 Aug 31;28(4):474-484. doi: 10.5607/en.2019.28.4.474.

Abstract

Absence seizures (AS) are generalized non-convulsive seizures characterized by a brief loss of consciousness and spike-and-wave discharges (SWD) in an electroencephalogram (EEG). A number of animal models have been developed to explain the mechanisms of AS, and thalamo-cortical networks are considered to be involved. However, the cortical foci have not been well described in mouse models of AS. This study aims to use a high density EEG in pathophysiologically different AS models to compare the spatiotemporal patterns of SWDs. We used two AS models: a pharmacologically induced model (gamma-hydroxybutyric acid, GHB model) and a transgenic model (phospholipase beta4 knock-out, PLCβ4 model). The occurrences of SWDs were confirmed by thalamic recordings. The topographical analysis of SWDs showed that the onset and propagation patterns were markedly distinguishable between the two models. In the PLCβ4 model, the foci were located within the somatosensory cortex followed by propagation to the frontal cortex, whereas in the GHB model, a majority of SWDs was initiated in the prefrontal cortex followed by propagation to the posterior cortex. In addition, in the GHB model, foci were also observed in other cortical areas. This observation indicates that different cortical networks are involved in the generation of SWDs across the two models.

摘要

失神发作(AS)是一种全身性非惊厥性发作,其特征为短暂意识丧失以及脑电图(EEG)中的棘慢波放电(SWD)。已经开发了许多动物模型来解释AS的机制,并且丘脑皮质网络被认为与之相关。然而,在AS小鼠模型中,皮质病灶尚未得到充分描述。本研究旨在使用高密度脑电图,在病理生理不同的AS模型中比较SWD的时空模式。我们使用了两种AS模型:一种药物诱导模型(γ-羟基丁酸,GHB模型)和一种转基因模型(磷脂酶β4基因敲除,PLCβ4模型)。通过丘脑记录确认了SWD的发生。SWD的地形分析表明,两种模型之间发作和传播模式明显不同。在PLCβ4模型中,病灶位于体感皮层内,随后传播至额叶皮层,而在GHB模型中,大多数SWD始于前额叶皮层,随后传播至后皮层。此外,在GHB模型中还在其他皮质区域观察到病灶。这一观察结果表明,两种模型中SWD的产生涉及不同皮质网络。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d5/6751861/a1781d1c01aa/en-28-474-g001.jpg

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