Journal
GENETICS
Volume 206, Issue 4, Pages 1739-1746Publisher
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.116.194779
Keywords
sodium channel; epilepsy; seizure-suppression; red light activable channelrhodopsin
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Funding
- McKnight Foundation
- National Institutes of Health [NS31231]
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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.
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