ArticleCerebral cortex (New York, N.Y. : 1991)2020
Increase in Seizure Susceptibility After Repetitive Concussion Results from Oxidative Stress, Parvalbumin-Positive Interneuron Dysfunction and Biphasic Increases in Glutamate/GABA Ratio.
Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Observational
- Extracellular matrix remodelling in neurological diseases.Nature reviews. Neurology · 2026Review
- Organophosphate Chemical Nerve Agents, Oxidative Stress, and NADPH Oxidase Inhibitors: An Overview.International journal of molecular sciences · 2025Review
- Review
- New epilepsy therapies in development.Nature reviews. Drug discovery · 2024Review
- An Open-Source Mouse Chronic EEG Array System with High-Density MXene-Based Skull Surface Electrodes.eNeuro · 2024Article
- Hippocampal interneuronal dysfunction and hyperexcitability in a porcine model of concussion.Communications biology · 2023Article
- Depressed glutamate transporter 1 expression in a mouse model of Dravet syndrome.Annals of clinical and translational neurology · 2023Article
- Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis.CNS neuroscience & therapeutics · 2023Review
- Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism.Neurochemical research · 2023Review
- Novel neuroendocrine role of γ-aminobutyric acid and gastrin-releasing peptide in the host response to influenza infection.Mucosal immunology · 2023Article
- N-acetylcysteine treatment mitigates loss of cortical parvalbumin-positive interneuron and perineuronal net integrity resulting from persistent oxidative stress in a rat TBI model.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023Review
- Somatostatin interneurons exhibit enhanced functional output and resilience to axotomy after mild traumatic brain injury.Neurobiology of disease · 2022Article
- Observational
- Structural changes in the neocortex as correlates of variations in EEG spectra and seizure susceptibility in rat brains with different degrees of dysplasia.The Journal of comparative neurology · 2022Article
- Increased seizure sensitivity in pregnant mice with genetic knockdown of acid sensing ion channel 2a is associated with impaired hippocampal inflammatory response.Frontiers in physiology · 2022Article
- Factors influencing the acute pentylenetetrazole-induced seizure paradigm and a literature review.Annals of clinical and translational neurology · 2021Review
- Article
- EEG markers predictive of epilepsy risk in pediatric cerebral malaria - A feasibility study.Epilepsy & behavior : E&B · 2020Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Chronic symptoms indicating excess cortical excitability follow mild traumatic brain injury, particularly repetitive mild traumatic brain injury (rmTBI). Yet mechanisms underlying post-traumatic excitation/inhibition (E/I) ratio abnormalities may differ between the early and late post-traumatic phases. We therefore measured seizure threshold and cortical gamma-aminobutyric acid (GABA) and glutamate (Glu) concentrations, 1 and 6 weeks after rmTBI in mice. We also analyzed the structure of parvalbumin-positive interneurons (PVIs), their perineuronal nets (PNNs), and their electroencephalography (EEG) signature (gamma frequency band power). For mechanistic insight, we measured cortical oxidative stress, reflected in the reduced/oxidized glutathione (GSH/GSSG) ratio. We found that seizure susceptibility increased both early and late after rmTBI. However, whereas increased Glu dominated the E/I 1 week after rmTBI, Glu concentration normalized and the E/I was instead characterized by depressed GABA, reduced per-PVI parvalbumin expression, and reduced gamma EEG power at the 6-week post-rmTBI time point. Oxidative stress was increased early after rmTBI, where transient PNN degradation was noted, and progressed throughout the monitoring period. We conclude that GSH depletion, perhaps triggered by early Glu-mediated excitotoxicity, leads to late post-rmTBI loss of PVI-dependent cortical inhibitory tone. We thus propose dampening of Glu signaling, maintenance of redox state, and preservation of PVI inhibitory capacity as therapeutic targets for post-rmTBI treatment.
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