title: Resistance of optogenetically evoked motor function to global ischemia and reperfusion in mouse in vivo.
abstract: Recently we have shown that despite reperfusion, sensory processing exhibits persistent deficits after global ischemia in a mouse in vivo model. We now address how motor output, specifically cortically evoked muscle activity, stimulated by channelrhodopsin-2 is affected by global ischemia and reperfusion. We find that the light-based optogenetic motor map recovers to 80% within an hour. Moreover, motor output recovers relatively faster and more completely than the sensory processing after 5-minute period of global ischemia. Our results suggest a differential sensitivity of sensory and motor systems to the effects of global ischemia and reperfusion that may have implications for rehabilitation.
authors.affiliation: Department of Psychiatry, Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada.
authors.forename: Yicheng
authors.initials: Y
authors.lastname: Xie
authors.forename: Shangbin
authors.initials: S
authors.lastname: Chen
authors.forename: Eitan
authors.initials: E
authors.lastname: Anenberg
authors.forename: Timothy H
authors.initials: TH
authors.lastname: Murphy
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D001931:Brain Mapping; D000075402:Channelrhodopsins; D004569:Electroencephalography; D004576:Electromyography; D007834:Lasers; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D059906:Neuroimaging; D010812:Physical Stimulation; D015427:Reperfusion Injury / Q000503:physiopathology*
chemical_list: D000075402:Channelrhodopsins