ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Ministrokes in channelrhodopsin-2 transgenic mice reveal widespread deficits in motor output despite maintenance of cortical neuronal excitability.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Hemodynamic and Electrophysiological Progression of the Rose Bengal Photothrombotic Stroke Model in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Neuronal injuries in cerebral infarction and ischemic stroke: From mechanisms to treatment (Review).International journal of molecular medicine · 2022Review
- A simulation study investigating potential diffusion-based MRI signatures of microstrokes.Scientific reports · 2021Article
- Review
- Multimodal mapping of neural activity and cerebral blood flow reveals long-lasting neurovascular dissociations after small-scale strokes.Science advances · 2020Article
- Recovery from cortical blindness with mepivacaïne.Annals of clinical and translational neurology · 2019Article
- Juxtacortical lesions are associated with seizures in cerebral small vessel disease.Journal of neurology · 2019Article
- Functional deficits induced by cortical microinfarcts.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Detection, risk factors, and functional consequences of cerebral microinfarcts.The Lancet. Neurology · 2017Review
- Multiparametric Imaging of Organ System Interfaces.Circulation. Cardiovascular imaging · 2017Review
- Neurorestoration after stroke.Neurosurgical focus · 2016Review
- Re-Establishment of Cortical Motor Output Maps and Spontaneous Functional Recovery via Spared Dorsolaterally Projecting Corticospinal Neurons after Dorsal Column Spinal Cord Injury in Adult Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Optogenetic Approaches to Target Specific Neural Circuits in Post-stroke Recovery.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- Novel Stroke Therapeutics: Unraveling Stroke Pathophysiology and Its Impact on Clinical Treatments.Neuron · 2015Review
- Robust and fragile aspects of cortical blood flow in relation to the underlying angioarchitecture.Microcirculation (New York, N.Y. : 1994) · 2015Review
- Optogenetic neuronal stimulation promotes functional recovery after stroke.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
We evaluated the effects of ministrokes targeted to individual pial arterioles on motor function in Thy-1 line 18 channelrhodopsin-2 (ChR2) transgenic mice within the first hours after ischemia. Using optogenetics, we directly assessed both the excitability and motor output of cortical neurons in a manner independent of behavioral state or training. Occlusion of individual arterioles within the motor cortex led to a ministroke that was verified using laser speckle contrast imaging. Surprisingly, ministrokes targeted to a relatively small region of the forelimb motor map, with an ischemic core of 0.07 ± 0.03 mm(2), impaired motor responses evoked from points across widespread areas of motor cortex even 1.5 mm away. Contrasting averaged ChR2-evoked electroencephalographic, spinal (ChR2 evoked potential), and electromyographic responses revealed a mismatch between measures of cortical excitability and motor output within 60 min after stroke. This mismatch suggests that apparently excitable cortical neurons (even >1 mm into peri-infarct areas, away from the infarct core) were impaired in their capacity to generate spinal potentials leading to even more severe deficits in motor output at muscles. We suggest that ischemia, targeted to a subset of motor cortex, leads to relatively small reductions in excitability within motor cortex, and cumulative depression of both descending spinal circuits and motor output in response to the activation of widespread cortical territories even outside of the area directly affected by the ischemia.
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Registered trials
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