ArticleExperimental neurology2016
Primary blast injury causes cognitive impairments and hippocampal circuit alterations.
Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Spatial Transcriptomics and Dual Dye Mapping Identify Wnt-Driven BBB Protection in Endothelial EphA4-Deficiency.Research square · 2026Article
- Article
- In silico investigation of brain tissue responses associated with mild blast traumatic brain injury.Frontiers in bioengineering and biotechnology · 2026Article
- PP2A methylesterase, PME-1, and PP2A methyltransferase, LCMT-1, control sensitivity to impairments caused by injury-related oligomeric tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology.International journal of molecular sciences · 2025Review
- Chronic Neurobehavioral and Neuropathological Consequences of Repeated Blast Exposure in P301S Transgenic Tau Rats.Neurotrauma reports · 2025Article
- Ryanodex Reduces Persistent Hippocampal Effects of Single Mild Traumatic Brain Injury in Rats.Neurotrauma reports · 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
- Multifunctional redox modulator prevents blast-induced loss of cochlear and vestibular hair cells and auditory spiral ganglion neurons.Scientific reports · 2024Article
- Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure.Frontiers in neuroscience · 2024Review
- Twenty Years of Blast-Induced Neurotrauma: Current State of Knowledge.Neurotrauma reports · 2024Article
- Repetitive, but Not Single, Mild Blast TBI Causes Persistent Neurological Impairments and Selective Cortical Neuronal Loss in Rats.Brain sciences · 2023Article
- Sustained Hippocampal Synaptic Pathophysiology Following Single and Repeated Closed-Head Concussive Impacts.Frontiers in cellular neuroscience · 2021Article
- Characterization of the Jet-Flow Overpressure Model of Traumatic Brain Injury in Mice.Neurotrauma reports · 2021Article
- Concussion increases CA1 activity during prolonged inactivity in a familiar environment.Experimental neurology · 2020Article
- Multi-Dimensional Mapping of Brain-Derived Extracellular Vesicle MicroRNA Biomarker for Traumatic Brain Injury Diagnostics.Journal of neurotrauma · 2020Article
- Behavioral Deficits in Animal Models of Blast Traumatic Brain Injury.Frontiers in neurology · 2020Review
- Neurodegeneration exposes firing rate dependent effects on oscillation dynamics in computational neural networks.PloS one · 2020Article
- Diagnosis of traumatic brain injury using miRNA signatures in nanomagnetically isolated brain-derived extracellular vesicles.Lab on a chip · 2018Article
- Blast-Induced Traumatic Brain Injury Triggered by Moderate Intensity Shock Wave Using a Modified Experimental Model of Injury in Mice.Chinese medical journal · 2018Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Blast-induced traumatic brain injury (bTBI) and its long term consequences are a major health concern among veterans. Despite recent work enhancing our knowledge about bTBI, very little is known about the contribution of the blast wave alone to the observed sequelae. Herein, we isolated its contribution in a mouse model by constraining the animals' heads during exposure to a shockwave (primary blast). Our results show that exposure to primary blast alone results in changes in hippocampus-dependent behaviors that correspond with electrophysiological changes in area CA1 and are accompanied by reactive gliosis. Specifically, five days after exposure, behavior in an open field and performance in a spatial object recognition (SOR) task were significantly different from sham. Network electrophysiology, also performed five days after injury, demonstrated a significant decrease in excitability and increase in inhibitory tone. Immunohistochemistry for GFAP and Iba1 performed ten days after injury showed a significant increase in staining. Interestingly, a threefold increase in the impulse of the primary blast wave did not exacerbate these measures. However, we observed a significant reduction in the contribution of the NMDA receptors to the field EPSP at the highest blast exposure level. Our results emphasize the need to account for the effects of primary blast loading when studying the sequelae of bTBI.
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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.