Investigation of Seizure-Susceptibility in a Drosophila melanogaster Model of Human Epilepsy with Optogenetic Stimulation

被引：11

作者：

Saras, Arunesh ^{[1
]}

Wu, Veronica V. ^{[1
]}

Brawer, Harlan J. ^{[1
]}

Tanouye, Mark A. ^{[1
,2
]}

机构：

[1] Univ Calif Berkeley, Div Organismal Biol, Dept Environm Sci Policy & Management, Berkeley, CA 94720 USA

[2] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

来源：

GENETICS | 2017年 / 206卷 / 04期

基金：

美国国家卫生研究院;

关键词：

sodium channel; epilepsy; seizure-suppression; red light activable channelrhodopsin; SENSITIVE PARALYTIC MUTANTS; ONSET EPISODIC ATAXIA; SODIUM-CHANNEL GENE; MUSHROOM BODY; NEONATAL EPILEPSY; OLFACTORY MEMORY; NEURAL CIRCUITS; BEHAVIOR; ACTIVATION; NEURONS;

D O I：

10.1534/genetics.116.194779

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

We examined seizure-susceptibility in a Drosophila model of human epilepsy using optogenetic stimulation of ReaChR (red-activatable channelrhodopsin). Photostimulation of the seizure-sensitive mutant para(bss1) causes behavioral paralysis that resembles paralysis caused by mechanical stimulation, in many aspects. Electrophysiology shows that photostimulation evokes abnormal seizure-like neuronal firing in para(bss1) followed by a quiescent period resembling synaptic failure and apparently responsible for paralysis. The pattern of neuronal activity concludes with seizure-like activity just prior to recovery. We tentatively identify the mushroom body as one apparent locus of optogenetic seizure initiation. The alpha/beta lobes may be primarily responsible for mushroom body seizure induction.

引用

页码：1739 / 1746

页数：8

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