ArticleCerebral cortex (New York, N.Y. : 1991)2015
Traumatic Brain Injury Increases Cortical Glutamate Network Activity by Compromising GABAergic Control.
Article in Cerebral cortex (New York, N.Y. : 1991), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed.
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- Trial
- Methods for a bioengineered 3D human brain-like tissue model of neuroregeneration after traumatic brain injury.Neural regeneration research · 2026Article
- Review
- Deep cerebellar stimulation restores chronic motor deficits and loss of GABAergic neurons following sensorimotor cortex surgical brain injury in female rats.Experimental neurology · 2026Article
- Myelin sheaths persist for weeks following axon degeneration.Science advances · 2026Article
- Inhibitory GABAergic Neuron Loss due to Oxidative Damage During Ex Vivo Acute Brain Slice Preparation Influences Genesis and Dynamics of Epileptiform Activity.Journal of neurochemistry · 2026Article
- Hippocampal Interneurons Shape Spatial Coding Alterations in Neurological Disorders.Molecular neurobiology · 2025Review
- Functional Alterations in Parvalbumin-Positive Interneurons after Traumatic Brain Injury in Somatosensory Cortex of Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Sex differences in neuropathological response to traumatic brain injury: increased neuronal loss and astrogliosis in females.Brain structure & function · 2025Article
- Medial ganglionic eminence transplantation restores inhibition after central visual system brain injury.PNAS nexus · 2025Article
- Glutamate uptake is transiently compromised in the perilesional cortex following controlled cortical impact.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Imaging the large-scale and cellular response to focal traumatic brain injury in mouse neocortex.Experimental physiology · 2025Article
- Oligodendrocyte precursor cells facilitate neuronal lysosome release.Nature communications · 2025Article
- Mechanically-adaptive, resveratrol-eluting neural probes for improved intracortical recording performance and stability.Npj flexible electronics · 2025Article
- Alterations in topology, cost, and dynamics of gamma-band EEG functional networks in a preclinical model of traumatic brain injury.Network neuroscience (Cambridge, Mass.) · 2025Article
- Imaging the large-scale and cellular response to focal traumatic brain injury in mouse neocortex.bioRxiv : the preprint server for biology · 2024Article
- Feasibility and acceptability for LION, a fully remote, randomized clinical trial within the VA for light therapy to improve sleep in Veterans with and without TBI: An MTBImedRxiv : the preprint server for health sciences · 2024Article
- Insights into epileptogenesis from post-traumatic epilepsy.Nature reviews. Neurology · 2024Review
- Pathological Interplay between Inflammation and Mitochondria Aggravates Glutamate Toxicity.International journal of molecular sciences · 2024Review
56 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
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Abstract
Traumatic brain injury (TBI) is a major risk factor for developing pharmaco-resistant epilepsy. Although disruptions in brain circuitry are associated with TBI, the precise mechanisms by which brain injury leads to epileptiform network activity is unknown. Using controlled cortical impact (CCI) as a model of TBI, we examined how cortical excitability and glutamatergic signaling was altered following injury. We optically mapped cortical glutamate signaling using FRET-based glutamate biosensors, while simultaneously recording cortical field potentials in acute brain slices 2-4 weeks following CCI. Cortical electrical stimulation evoked polyphasic, epileptiform field potentials and disrupted the input-output relationship in deep layers of CCI-injured cortex. High-speed glutamate biosensor imaging showed that glutamate signaling was significantly increased in the injured cortex. Elevated glutamate responses correlated with epileptiform activity, were highest directly adjacent to the injury, and spread via deep cortical layers. Immunoreactivity for markers of GABAergic interneurons were significantly decreased throughout CCI cortex. Lastly, spontaneous inhibitory postsynaptic current frequency decreased and spontaneous excitatory postsynaptic current increased after CCI injury. Our results suggest that specific cortical neuronal microcircuits may initiate and facilitate the spread of epileptiform activity following TBI. Increased glutamatergic signaling due to loss of GABAergic control may provide a mechanism by which TBI can give rise to post-traumatic epilepsy.
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