ArticleNeurobiology of disease2022
Low-intensity blast induces acute glutamatergic hyperexcitability in mouse hippocampus leading to long-term learning deficits and altered expression of proteins involved in synaptic plasticity and serine protease inhibitors.
Article in Neurobiology of disease, 2022. 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, 21 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Multi-omics analysis identified serumJournal of thoracic disease · 2026Article
- Immediate Consequences of a Spinal Cord Injury During Development: Unique Insights From Ex Vivo Models.Neural plasticity · 2026Review
- Proteomic analysis of plasma unravels dynamic pathways and potential biomarkers indicating disease stages followingmSystems · 2025Article
- UTE MRI for assessing demyelination in an mTBI mouse model: An open-field low-intensity blast study.NeuroImage · 2025Article
- Temporal changes of neurobehavior in rats following varied blast magnitudes and screening of serum biomarkers in early stage of brain injury.Scientific reports · 2024Article
- Modeling Highly Repetitive Low-level Blast Exposure in Mice.Journal of visualized experiments : JoVE · 2024Article
- Quantitative proteomic profiling in brain subregions of mice exposed to open-field low-intensity blast reveals position-dependent blast effects.Shock waves · 2024Article
- The Chronic Effects of a Single Low-Intensity Blast Exposure on Phosphoproteome Networks and Cognitive Function Influenced by Mutant Tau Overexpression.International journal of molecular sciences · 2024Article
- The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.International journal of molecular sciences · 2024Review
- Low-Intensity Blast Exposure Induces Multifaceted Long-Lasting Anxiety-Related Behaviors in Mice.Neurotrauma reports · 2024Article
- Individualized high-resolution analysis to categorize diverse learning and memory deficits in tau rTg4510 mice exposed to low-intensity blast.Frontiers in cellular neuroscience · 2024Article
- Blast-related mild TBI: LIMBIC-CENC focused review with implications commentary.NeuroRehabilitation · 2024Review
- Mitochondrial Dysfunction After Repeated Mild Blast Traumatic Brain Injury Is Attenuated by a Mild Mitochondrial Uncoupling Prodrug.Journal of neurotrauma · 2023Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Neurocognitive consequences of blast-induced traumatic brain injury (bTBI) pose significant concerns for military service members and veterans with the majority of "invisible injury." However, the underlying mechanism of such mild bTBI by low-intensity blast (LIB) exposure for long-term cognitive and mental deficits remains elusive. Our previous studies have shown that mice exposed to LIB result in nanoscale ultrastructural abnormalities in the absence of gross or apparent cellular damage in the brain. Here we tested the hypothesis that glutamatergic hyperexcitability may contribute to long-term learning deficits. Using brain slice electrophysiological recordings, we found an increase in averaged frequencies with a burst pattern of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal CA3 neurons in LIB-exposed mice at 1- and 7-days post injury, which was blocked by a specific NMDA receptor antagonist AP5. In addition, cognitive function assessed at 3-months post LIB exposure by automated home-cage monitoring showed deficits in dynamic patterns of discrimination learning and cognitive flexibility in LIB-exposed mice. Collected hippocampal tissue was further processed for quantitative global-proteomic analysis. Advanced data-independent acquisition for quantitative tandem mass spectrometry analysis identified altered expression of proteins involved in synaptic plasticity and serine protease inhibitors in LIB-exposed mice. Some were correlated with the ability of discrimination learning and cognitive flexibility. These findings show that acute glutamatergic hyperexcitability in the hippocampus induced by LIB may contribute to long-term cognitive dysfunction and protein alterations. Studies using this military-relevant mouse model of mild bTBI provide valuable insights into developing a potential therapeutic strategy to ameliorate hyperexcitability-modulated LIB injuries.
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