ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2019
Delayed inhibition of tonic inhibition enhances functional recovery following experimental ischemic stroke.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Impaired peri-infarct long-term potentiation in anaesthetized rats suggests alternative mechanisms of post-stroke recovery.The Journal of physiology · 2026Article
- Signatures of Covert Neuron Loss in the Local Field Potential of Motor Cortex.Journal of the American Heart Association · 2026Article
- The role of GABANeuroscience and biobehavioral reviews · 2026Review
- Peripheral B cell populations tune spontaneous neuronal activity in the uninjured hippocampus after stroke.bioRxiv : the preprint server for biology · 2026Article
- Microglia interact with dendritic spines and regulate spine numbers after brain injury following resuscitation from a cardiac arrest.Experimental neurology · 2025Article
- A place for place cells in post-stroke cognitive impairment.Trends in neurosciences · 2025Article
- A novel peptide inhibitor of TRPM2 channels improves recovery of memory function following traumatic brain injury.Frontiers in synaptic neuroscience · 2025Article
- Interventions for Neural Plasticity in Stroke Recovery.Archives of internal medicine research · 2025Article
- Delayed Fluoxetine Administration Restores Hippocampal Function in a Juvenile Global Cerebral Ischemia Mouse Model in a Sex-Specific Manner.Neural plasticity · 2025Article
- Article
- The Excessive Tonic Inhibition of the Peri-infarct Cortex Depresses Low Gamma Rhythm Power During Poststroke Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Considering Context-Specific microRNAs in Ischemic Stroke with Three "W": Where, When, and What.Molecular neurobiology · 2024Review
- TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Astrocyte Regulation of Neuronal Function and Survival in Stroke Pathophysiology.Advances in neurobiology · 2024Review
- Targeting BACE1-mediated production of amyloid beta improves hippocampal synaptic function in an experimental model of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Review
- Spectral slowing in chronic stroke reflects abnormalities in both periodic and aperiodic neural dynamics.NeuroImage. Clinical · 2023Article
- Neuron-targeted Knockout of APE1 Forces Premature Cognitive Impairment and Synaptic Dysfunction in Adult Mice.Aging and disease · 2022Article
- Cutaneous burn injury induces neuroinflammation and reactive astrocyte activation in the hippocampus of aged mice.Experimental gerontology · 2022Article
- Stepwise disassembly of GABAergic synapses during pathogenic excitotoxicity.Cell reports · 2021Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
The current study focuses on the ability to improve cognitive function after stroke with interventions administered at delayed/chronic time points. In light of recent studies demonstrating delayed GABA antagonists improve motor function, we utilized electrophysiology, biochemistry and neurobehavioral methods to investigate the role of α5 GABAA receptors on hippocampal plasticity and functional recovery following ischemic stroke. Male C57Bl/6 mice were exposed to 45 min transient middle cerebral artery occlusion and analysis of synaptic and functional deficits performed 7 or 30 days after recovery. Our findings indicate that hippocampal long-term potentiation (LTP) is impaired 7 days after stroke and remain impaired for at least 30 days. We demonstrate that ex vivo administration of L655,708 reversed ischemia-induced plasticity deficits and importantly, in vivo administration at delayed time-points reversed stroke-induced memory deficits. Western blot analysis of hippocampal tissue reveals proteins responsible for GABA synthesis are upregulated (GAD65/67 and MAOB), increasing GABA in hippocampal interneurons 30 days after stroke. Thus, our data indicate that both synaptic plasticity and memory impairments observed after stroke are caused by excessive tonic GABA activity, making inhibition of specific GABA activity at delayed timepoints a potential therapeutic approach to improve functional recovery and reverse cognitive impairments after stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.