Resistance of Optogenetically Evoked Motor Function to Global Ischemia and Reperfusion in Mouse <i>in Vivo</i>

Xie, Yicheng; Chen, Shangbin; Anenberg, Eitan; Murphy, Timothy H.

doi:10.1038/jcbfm.2013.89

Cited by 15 publications

(11 citation statements)

References 15 publications

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“…Tools to Shape the Connectome: Animal Models Optogenetics provides exquisite control over brain circuitry (Madisen et al, 2012). In the case of stroke, this technique provides (1) an effective means of probing brains of stroke-affected animals to understand the deficits associated with stroke (Anenberg et al, 2014;Chen et al, 2012;Xie et al, 2013), and (2) a platform to optimize effects of brain stimulation (Cheng et al, 2014), or inhibition on recovery that may be later attempted in humans using more clinically tractable means. To shape activity within the rodent connectome, investigators have a host of different optogenetic actuator and monitoring tools (Chen and Schlaug, 2013;Daniel et al, 2014;Madisen et al, 2012).…”

Section: How To Modify and Guide Connectome Changes Poststroke Inductmentioning

confidence: 99%

Stroke and the Connectome: How Connectivity Guides Therapeutic Intervention

Silasi

Murphy

2014

Neuron

192

146

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Connections between neurons are affected within 3 min of stroke onset by massive ischemic depolarization and then delayed cell death. Some connections can recover with prompt reperfusion; others associated with the dying infarct do not. Disruption in functional connectivity is due to direct tissue loss and indirect disconnections of remote areas known as diaschisis. Stroke is devastating, yet given the brain's redundant design, collateral surviving networks and their connections are well-positioned to compensate. Our perspective is that new treatments for stroke may involve a rational functional and structural connections-based approach. Surviving, affected, and at-risk networks can be identified and targeted with scenario-specific treatments. Strategies for recovery may include functional inhibition of the intact hemisphere, rerouting of connections, or setpoint-mediated network plasticity. These approaches may be guided by brain imaging and enabled by patient- and injury-specific brain stimulation, rehabilitation, and potential molecule-based strategies to enable new connections.

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Section: How To Modify and Guide Connectome Changes Poststroke Inductmentioning

confidence: 99%

Stroke and the Connectome: How Connectivity Guides Therapeutic Intervention

Silasi

Murphy

2014

Neuron

192

146

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“…After 15 min of forebrain ischemia, the clamps were removed to allow reperfusion. As the mice were anesthetized, EEG measurement was used (ElHayek et al, 2011;Xie et al, 2013). Only those mice showing completely flat electroencephalograms after vascular occlusion were classified as ischemic and used in the study.…”

Section: Cerebral Ischemia-reperfusion Injury Modelmentioning

confidence: 99%

Hypothermia-induced ischemic tolerance is associated with Drp1 inhibition in cerebral ischemia-reperfusion injury of mice

et al. 2016

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“…[4][5][6][7][8] Such a spatial approach in the cortex would build upon previous temporal approaches for studying the hemodynamic response with optogenetics. Laser speckle contrast imaging, [9][10][11] intrinsic optical signal imaging, 9,12,13 and functional magnetic resonance imaging (fMRI) [14][15][16] have been combined with temporal optogenetic modulation to investigate cerebral hemodynamics.…”

Section: Introductionmentioning

confidence: 99%

Patterned Optogenetic Modulation of Neurovascular and Metabolic Signals

Richner

Baumgartner

Brodnick

et al. 2014

J Cereb Blood Flow Metab

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The hemodynamic and metabolic response of the cortex depends spatially and temporally on the activity of multiple cell types. Optogenetics enables specific cell types to be modulated with high temporal precision and is therefore an emerging method for studying neurovascular and neurometabolic coupling. Going beyond temporal investigations, we developed a microprojection system to apply spatial photostimulus patterns in vivo. We monitored vascular and metabolic fluorescence signals after photostimulation in Thy1-channelrhodopsin-2 mice. Cerebral arteries increased in diameter rapidly after photostimulation, while nearby veins showed a slower smaller response. The amplitude of the arterial response was depended on the area of cortex stimulated. The fluorescence signal emitted at 450/100 nm and excited with ultraviolet is indicative of reduced nicotinamide adenine dinucleotide, an endogenous fluorescent enzyme involved in glycolysis and the citric acid cycle. This fluorescence signal decreased quickly and transiently after optogenetic stimulation, suggesting that glucose metabolism is tightly locked to optogenetic stimulation. To verify optogenetic stimulation of the cortex, we used a transparent substrate microelectrode array to map cortical potentials resulting from optogenetic stimulation. Spatial optogenetic stimulation is a new tool for studying neurovascular and neurometabolic coupling.

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Resistance of Optogenetically Evoked Motor Function to Global Ischemia and Reperfusion in Mouse in Vivo

Cited by 15 publications

References 15 publications

Stroke and the Connectome: How Connectivity Guides Therapeutic Intervention

Stroke and the Connectome: How Connectivity Guides Therapeutic Intervention

Hypothermia-induced ischemic tolerance is associated with Drp1 inhibition in cerebral ischemia-reperfusion injury of mice

Patterned Optogenetic Modulation of Neurovascular and Metabolic Signals

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