ArticleJournal of neurotrauma2016
Isolated Primary Blast Inhibits Long-Term Potentiation in Organotypic Hippocampal Slice Cultures.
Article in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Long-term potentiation and long-term depression are both impaired afterBiomedical physics & engineering express · 2025Article
- Partial Depletion of Microglia Attenuates Long-Term Potentiation Deficits following Repeated Blast Traumatic Brain Injury in Organotypic Hippocampal Slice Cultures.Journal of neurotrauma · 2023Article
- A novel organotypic cortical slice culture model for traumatic brain injury: molecular changes induced by injury and mesenchymal stromal cell secretome treatment.Frontiers in cellular neuroscience · 2023Article
- The Emergence of Model Systems to Investigate the Link Between Traumatic Brain Injury and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Perspectives on Primary Blast Injury of the Brain: Translational Insights Into Non-inertial Low-Intensity Blast Injury.Frontiers in neurology · 2021Review
- A Mouse Model of Repetitive Blast Traumatic Brain Injury Reveals Post-Trauma Seizures and Increased Neuronal Excitability.Journal of neurotrauma · 2020Article
- Incretin Mimetics as Rational Candidates for the Treatment of Traumatic Brain Injury.ACS pharmacology & translational science · 2019Article
- Cypin: A novel target for traumatic brain injury.Neurobiology of disease · 2018Article
- Xenon Protects against Blast-Induced Traumatic Brain Injury in an In Vitro Model.Journal of neurotrauma · 2018Article
- Phosphodiesterase-4 inhibition restored hippocampal long term potentiation after primary blast.Experimental neurology · 2017Article
- Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration.Scientific reports · 2017Article
- Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice cultures.PloS one · 2017Article
- Primary Blast-Induced Changes in Akt and GSKFrontiers in neurology · 2017Article
- Bioorthogonal chemical imaging of metabolic activities in live mammalian hippocampal tissues with stimulated Raman scattering.Scientific reports · 2016Article
- Primary Blast Exposure Increases Hippocampal Vulnerability to Subsequent Exposure: Reducing Long-Term Potentiation.Journal of neurotrauma · 2016Article
- Primary blast injury causes cognitive impairments and hippocampal circuit alterations.Experimental neurology · 2016Article
- Behavioral Outcomes Differ between Rotational Acceleration and Blast Mechanisms of Mild Traumatic Brain Injury.Frontiers in neurology · 2016Article
- A 6-Step Approach to Gain Higher Quality Results From Organotypic Hippocampal Brain Slices in a Traumatic Brain Injury Model.Basic and clinical neuroscienceArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Over the last 13 years, traumatic brain injury (TBI) has affected over 230,000 U.S. service members through the conflicts in Iraq and Afghanistan, mostly as a result of exposure to blast events. Blast-induced TBI (bTBI) is multi-phasic, with the penetrating and inertia-driven phases having been extensively studied. The effects of primary blast injury, caused by the shockwave interacting with the brain, remain unclear. Earlier in vivo studies in mice and rats have reported mixed results for primary blast effects on behavior and memory. Using a previously developed shock tube and in vitro sample receiver, we investigated the effect of isolated primary blast on the electrophysiological function of rat organotypic hippocampal slice cultures (OHSC). We found that pure primary blast exposure inhibited long-term potentiation (LTP), the electrophysiological correlate of memory, with a threshold between 9 and 39 kPa·ms impulse. This deficit occurred well below a previously identified threshold for cell death (184 kPa·ms), supporting our previously published finding that primary blast can cause changes in brain function in the absence of cell death. Other functional measures such as spontaneous activity, network synchronization, stimulus-response curves, and paired-pulse ratios (PPRs) were less affected by primary blast exposure, as compared with LTP. This is the first study to identify a tissue-level tolerance threshold for electrophysiological changes in neuronal function to isolated primary blast.
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Registered trials
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.