ArticleJournal of neurotrauma2015
Alterations in Hippocampal Network Activity after In Vitro Traumatic Brain Injury.
Article in Journal of neurotrauma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- A single mild closed-head injury disrupts synaptic strength and promotes hippocampal hyperexcitability in mice.Brain communications · 2026Article
- Long-term potentiation and long-term depression are both impaired afterBiomedical physics & engineering express · 2025Article
- Stretch-Induced Injury Affects Cortical Neuronal Networks in a Time- and Severity-Dependent Manner.Annals of biomedical engineering · 2024Article
- Commonly Overlooked Factors in Biocompatibility Studies of Neural Implants.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- 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
- A multilayer network model of neuron-astrocyte populations in vitro reveals mGluRNetwork neuroscience (Cambridge, Mass.) · 2022Article
- Flexibility ofFrontiers in cellular neuroscience · 2022Article
- Plasticity impairment alters community structure but permits successful pattern separation in a hippocampal network model.Frontiers in cellular neuroscience · 2022Article
- Lipopolysaccharide-induced neuroinflammation disrupts functional connectivity and community structure in primary cortical microtissues.Scientific reports · 2021Article
- Peering into the Brain through the Retrosplenial Cortex to Assess Cognitive Function of the Injured Brain.Neurotrauma reports · 2021Article
- The Emergence of Model Systems to Investigate the Link Between Traumatic Brain Injury and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- A soft and stretchable bilayer electrode array with independent functional layers for the next generation of brain machine interfaces.Journal of neural engineering · 2020Article
- CurrentCurrent opinion in biomedical engineering · 2020Article
- High-speed mechano-active multielectrode array for investigating rapid stretch effects on cardiac tissue.Nature communications · 2019Article
- Phosphodiesterase-4 inhibition restored hippocampal long term potentiation after primary blast.Experimental neurology · 2017Article
- Role of Akt-independent mTORC1 and GSK3β signaling in sublethal NMDA-induced injury and the recovery of neuronal electrophysiology and survival.Scientific reports · 2017Article
- Role of Wnt Signaling in Central Nervous System Injury.Molecular neurobiology · 2016Review
- Isolated Primary Blast Inhibits Long-Term Potentiation in Organotypic Hippocampal Slice Cultures.Journal of neurotrauma · 2016Article
- Hippocampal Neurophysiologic Changes after Mild Traumatic Brain Injury and Potential Neuromodulation Treatment Approaches.Frontiers in systems neuroscience · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) alters function and behavior, which can be characterized by changes in electrophysiological function in vitro. A common cognitive deficit after mild-to-moderate TBI is disruption of persistent working memory, of which the in vitro correlate is long-lasting, neuronal network synchronization that can be induced pharmacologically by the gamma-aminobutyric acid A antagonist, bicuculline. We utilized a novel in vitro platform for TBI research, the stretchable microelectrode array (SMEA), to investigate the effects of TBI on bicuculline-induced, long-lasting network synchronization in the hippocampus. Mechanical stimulation significantly disrupted bicuculline-induced, long-lasting network synchronization 24 h after injury, despite the continued ability of the injured neurons to fire, as revealed by a significant increase in the normalized spontaneous event rate in the dentate gyrus (DG) and CA1. A second challenge with bicuculline 24 h after the first challenge significantly decreased the normalized spontaneous event rate in the DG. In addition, we illustrate the utility of the SMEA for TBI research by combining multiple experimental paradigms in one platform, which has the potential to enable novel investigations into the mechanisms responsible for functional consequences of TBI and speed the rate of drug discovery.
Indexed as
Identifiers
What OpenQuestion holds
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.