ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Optogenetic analysis of neuronal excitability during global ischemia reveals selective deficits in sensory processing following reperfusion in mouse cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Article
- Comparative Study of Terminal Cortical Potentials Using Iridium and Ag/AgCl Electrodes.International journal of molecular sciences · 2023Article
- Depth-profile of impairments in endothelin-1 - induced focal cortical ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Cholinergic upregulation by optogenetic stimulation of nucleus basalis after photothrombotic stroke in forelimb somatosensory cortex improves endpoint and motor but not sensory control of skilled reaching in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Optogenetic Interrogation of Circuits Following Neurotrauma.Frontiers in molecular neuroscience · 2021Review
- Intranasal erythropoietin ameliorates neurological function impairments and neural pathology in mice with chronic alcoholism by regulating autophagy‑related Nrf2 degradation.Molecular medicine reports · 2019Article
- Optogenetic Approaches to Target Specific Neural Circuits in Post-stroke Recovery.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- Optogenetic stimulation of GABA neurons can decrease local neuronal activity while increasing cortical blood flow.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Chloride Cotransporters as a Molecular Mechanism underlying Spreading Depolarization-Induced Dendritic Beading.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Prolonged deficits in parvalbumin neuron stimulation-evoked network activity despite recovery of dendritic structure and excitability in the somatosensory cortex following global ischemia in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Optogenetic neuronal stimulation promotes functional recovery after stroke.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Ministrokes in channelrhodopsin-2 transgenic mice reveal widespread deficits in motor output despite maintenance of cortical neuronal excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Indian-ink perfusion based method for reconstructing continuous vascular networks in whole mouse brain.PloS one · 2014Article
- Uncoupling PSD-95 interactions leads to rapid recovery of cortical function after focal stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
- Resistance of optogenetically evoked motor function to global ischemia and reperfusion in mouse in vivo.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
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4 authors.
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Abstract
We have developed an approach to directly probe neuronal excitability during the period beginning with induction of global ischemia and extending after reperfusion using transgenic mice expressing channelrhodopsin-2 (ChR2) to activate deep layer cortical neurons independent of synaptic or sensory stimulation. Spontaneous, ChR2, or forepaw stimulation-evoked electroencephalogram (EEG) or local field potential (LFP) records were collected from the somatosensory cortex. Within 20 s of ischemia, a >90% depression of spontaneous 0.3-3 Hz EEG and LFP power was detected. Ischemic depolarization followed EEG depression with a ∼2 min delay. Surprisingly, neuronal excitability, as assessed by the ChR2-mediated EEG response, was intact during the period of strong spontaneous EEG suppression and actually increased before ischemic depolarization. In contrast, a decrease in the somatosensory-evoked potential (forepaw-evoked potential, reflecting cortical synaptic transmission) was coincident with the EEG suppression. After 5 min of ischemia, the animal was reperfused, and the ChR2-mediated response mostly recovered within 30 min (>80% of preischemia value). However, the recovery of the somatosensory-evoked potential was significantly delayed compared with the ChR2-mediated response (<40% of preischemia value at 60 min). By assessing intrinsic optical signals in combination with EEG, we found that neuronal excitability approached minimal values when the spreading ischemic depolarization wave propagated to the ChR2-stimulated cortex. Our results indicate that the ChR2-mediated EEG/LFP response recovers much faster than sensory-evoked EEG/LFP activity in vivo following ischemia and reperfusion, defining a period where excitable but synaptically silent neurons are present.
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