ArticleExperimental neurology2020
Chemogenetics-mediated acute inhibition of excitatory neuronal activity improves stroke outcome.
Article in Experimental neurology, 2020. 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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15 citing papers in PubMed, 23 citations in OpenAlex.
- PKM2 from hyperactive neuron aggravate lung injury post-stroke by promoting FOXO3A/TXNIP mitochondria translocation in mice.Redox biology · 2026Article
- Cortical spreading depolarizations in stroke: Mechanisms, neuroprotective interventions, and monitoring techniques.GeroScience · 2026Review
- CaMKII Neurons in the Dentate Gyrus Are Involved in Regulating Cognitive Impairment in Mice Induced by Stress Caused by Violence.International journal of molecular sciences · 2025Article
- Cutting-edge technologies in neural regeneration.Cell regeneration (London, England) · 2025Review
- Aberrant neuronal excitation promotes neuroinflammation in the primary motor cortex of ischemic stroke mice.Acta pharmacologica Sinica · 2025Article
- Activation of the PERK Branch of the UPR as a Strategy for Improving Outcomes in Acute Ischemic Stroke.ACS omega · 2025Article
- Electrophysiological Signatures in Global Cerebral Ischemia: Neuroprotection Via Chemogenetic Inhibition of CA1 Pyramidal Neurons in Rats.Journal of the American Heart Association · 2024Article
- Article
- MiR-100-5p-rich small extracellular vesicles from activated neuron to aggravate microglial activation and neuronal activity after stroke.Journal of nanobiotechnology · 2024Article
- Exogenous Functional Mitochondria Derived from Bone Mesenchymal Stem Cells That Respond to ROS Can Rescue Neural Cells Following Ischemic Stroke.Journal of inflammation research · 2024Article
- Clozapine-Induced Chemogenetic Neuromodulation Rescues Post-Stroke Deficits After Chronic Capsular Infarct.Translational stroke research · 2023Article
- A Linarin Derivative Protects against Ischemia-Induced Neuronal Injury in Mice by Promoting Cerebral Blood Flow Recovery via KDELR-Dependent CSPG4 Activation.Oxidative medicine and cellular longevity · 2022Article
- Review
- Phase-specific manipulation of neuronal activity: a promising stroke therapy approach.Neural regeneration research · 2021Article
- Chronic nicotine impairs sparse motor learning via striatal fast-spiking parvalbumin interneurons.Addiction biology · 2021Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeIschemic stroke significantly perturbs neuronal homeostasis leading to a cascade of pathologic events causing brain damage. In this study, we assessed acute stroke outcome after chemogenetic inhibition of forebrain excitatory neuronal activity.
methodsWe generated hM4Di-TG transgenic mice expressing the inhibitory hM4Di, a Designer Receptors Exclusively Activated by Designer Drugs (DREADD)-based chemogenetic receptor, in forebrain excitatory neurons. Clozapine-N-oxide (CNO) was used to activate hM4Di DREADD. Ischemic stroke was induced by transient occlusion of the middle cerebral artery. Neurologic function and infarct volumes were evaluated. Excitatory neuronal suppression in the hM4Di-TG mouse forebrain was assessed electrophysiologically in vitro and in vivo, based on evoked synaptic responses, and in vivo based on occurrence of potassium-induced cortical spreading depolarizations.
resultsDetailed characterization of hM4Di-TG mice confirmed that evoked synaptic responses in both in vitro hippocampal slices and in vivo motor cortex were significantly reduced after CNO-mediated activation of the inhibitory hM4Di DREADD. Further, CNO treatment had no obvious effects on physiology and motor function in either control or hM4Di-TG mice. Importantly, hM4Di-TG mice treated with CNO at either 10 min before ischemia or 30 min after reperfusion exhibited significantly improved neurologic function and smaller infarct volumes compared to CNO-treated control mice. Mechanistically, we showed that potassium-induced cortical spreading depression episodes were inhibited, including frequency and duration of DC shift, in CNO-treated hM4Di-TG mice.
conclusionsOur data demonstrate that acute inhibition of a subset of excitatory neurons after ischemic stroke can prevent brain injury and improve functional outcome. This study, together with the previous work in optogenetic neuronal modulation during the chronic phase of stroke, supports the notion that targeting neuronal activity is a promising strategy in stroke therapy.
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