ArticleExperimental neurology2015
GABAergic interneuronal loss and reduced inhibitory synaptic transmission in the hippocampal CA1 region after mild traumatic brain injury.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 83 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Investigating genetic susceptibility to concussion through rare variants in ion channel and neurotransmission genes.Journal of neurology · 2026Article
- Time-Dependent Diagnostic Windows After Isolated Diffuse Axonal Brain Injury in Rats.Diagnostics (Basel, Switzerland) · 2026Article
- The role of GABANeuroscience and biobehavioral reviews · 2026Review
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- Traumatic Brain Injury and Endocytosis: Reduced Rodent Hippocampal Endocytosis Proteins and Human Clathrin Light Chain Polymorphisms Are Associated with Impaired Neurological Outcomes After TBI.Molecular neurobiology · 2026Article
- A Novel NLRP3 Inhibitor AMS-17 Rescues Deficits in Long-Term Potentiation Following Mild Traumatic Brain Injury in Adult C57Bl/6 Mice.Hippocampus · 2026Article
- Hippocampal Interneurons Shape Spatial Coding Alterations in Neurological Disorders.Molecular neurobiology · 2025Review
- The effect of traumatic brain injury on learning and memory: A synaptic focus.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Medial ganglionic eminence transplantation restores inhibition after central visual system brain injury.PNAS nexus · 2025Article
- Exploring cerebral structural and functional abnormalities in a mouse model of post-traumatic headache induced by mild traumatic brain injury.Zoological research · 2024Article
- Bumetanide induces post-traumatic microglia-interneuron contact to promote neurogenesis and recovery.Brain : a journal of neurology · 2023Article
- The Rehabilitation Potential of Neurostimulation for Mild Traumatic Brain Injury in Animal and Human Studies.Brain sciences · 2023Review
- Gestational dexamethasone exposure impacts hippocampal excitatory synaptic transmission and learning and memory function with transgenerational effects.Acta pharmaceutica Sinica. B · 2023Article
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- Article
- Repetitive mild traumatic brain injury induces persistent alterations in spontaneous synaptic activity of hippocampal CA1 pyramidal neurons.IBRO neuroscience reports · 2022Article
- GABAInternational journal of molecular sciences · 2022Article
- Pharmacological modulation of cytokines correlating neuroinflammatory cascades in epileptogenesis.Molecular biology reports · 2022Review
- Stepwise disassembly of GABAergic synapses during pathogenic excitotoxicity.Cell reports · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Patients that suffer mild traumatic brain injuries (mTBI) often develop cognitive impairments, including memory and learning deficits. The hippocampus shows a high susceptibility to mTBI-induced damage due to its anatomical localization and has been implicated in cognitive and neurological impairments after mTBI. However, it remains unknown whether mTBI cognitive impairments are a result of morphological and pathophysiological alterations occurring in the CA1 hippocampal region. We investigated whether mTBI induces morphological and pathophysiological alterations in the CA1 using the controlled cortical impact (CCI) model. Seven days after CCI, animals subjected to mTBI showed cognitive impairment in the passive avoidance test and deficits to long-term potentiation (LTP) of synaptic transmission. Deficiencies in inducing or maintaining LTP were likely due to an observed reduction in the activation of NMDA but not AMPA receptors. Significant reductions in the frequency and amplitude of spontaneous and miniature GABAA-receptor mediated inhibitory postsynaptic currents (IPSCs) were also observed 7 days after CCI. Design-based stereology revealed that although the total number of neurons was unaltered, the number of GABAergic interneurons is significantly reduced in the CA1 region 7 days after CCI. Additionally, the surface expression of α1, ß2/3, and γ2 subunits of the GABAA receptor were reduced, contributing to a reduced mIPSC frequency and amplitude, respectively. Together, these results suggest that mTBI causes a significant reduction in GABAergic inhibitory transmission and deficits to NMDA receptor mediated currents in the CA1, which may contribute to changes in hippocampal excitability and subsequent cognitive impairments after mTBI.
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