ArticleFrontiers in cellular neuroscience2019
Rapid Changes in Synaptic Strength After Mild Traumatic Brain Injury.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- In People With Subacute Mild Traumatic Brain Injury, Earlier Physical Therapy Improved Symptoms at a Faster Rate Than Later Physical Therapy: Randomized Controlled Trial.Physical therapy · 2025Trial
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Effects of noninvasive brain stimulation on motor functions in animal models of ischemia and trauma in the central nervous system.Neural regeneration research · 2026Article
- A single mild closed-head injury disrupts synaptic strength and promotes hippocampal hyperexcitability in mice.Brain communications · 2026Article
- High frequency head impact exposure changes hippocampal sharp-wave ripple architecture.PloS one · 2026Article
- Article
- Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.International journal of molecular sciences · 2025Review
- Repetitive concussions promote microglia-mediated engulfment of presynaptic excitatory input associated with cognitive dysfunction.Communications biology · 2025Article
- Nano-scaffold containing functional motif of stromal cell-derived factor 1 enhances neural stem cell behavior and synaptogenesis in traumatic brain injury.Scientific reports · 2025Article
- Neurophysiological signatures of mild traumatic brain injury in the acute and subacute phase.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Complement propagates visual system pathology following traumatic brain injury.Journal of neuroinflammation · 2024Article
- Single Nucleotide Polymorphism in Cell Adhesion Molecule L1 Affects Learning and Memory in a Mouse Model of Traumatic Brain Injury.International journal of molecular sciences · 2024Article
- EEG hyperexcitability and hyperconnectivity linked to GABAergic inhibitory interneuron loss following traumatic brain injury.Brain communications · 2024Article
- Traumatic brain injuries: a neuropsychological review.Frontiers in behavioral neuroscience · 2024Review
- 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 mechanistic model of calcium homeostasis leading to occurrence and propagation of secondary brain injury.Journal of neurophysiology · 2022Article
- Repetitive mild traumatic brain injury induces persistent alterations in spontaneous synaptic activity of hippocampal CA1 pyramidal neurons.IBRO neuroscience reports · 2022Article
- 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.Neurobiology of disease · 2022Article
- Assessment of behavioral, neuroinflammatory, and histological responses in a model of rat repetitive mild fluid percussion injury at 2 weeks post-injury.Frontiers in neurology · 2022Article
- Repetitive mild traumatic brain injury in mice triggers a slowly developing cascade of long-term and persistent behavioral deficits and pathological changes.Acta neuropathologica communications · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) affects millions of Americans annually, but effective treatments remain inadequate due to our poor understanding of how injury impacts neural function. Data are particularly limited for mild, closed-skull TBI, which forms the majority of human cases, and for acute injury phases, when trauma effects and compensatory responses appear highly dynamic. Here we use a mouse model of mild TBI to characterize injury-induced synaptic dysfunction, and examine its progression over the hours to days after trauma. Mild injury consistently caused both locomotor deficits and localized neuroinflammation in piriform and entorhinal cortices, along with reduced olfactory discrimination ability. Using whole-cell recordings to characterize synaptic input onto piriform pyramidal neurons, we found moderate effects on excitatory or inhibitory synaptic function at 48 h after TBI and robust increase in excitatory inputs in slices prepared 1 h after injury. Excitatory increases predominated over inhibitory effects, suggesting that loss of excitatory-inhibitory balance is a common feature of both mild and severe TBI. Our data indicate that mild injury drives rapidly evolving alterations in neural function in the hours following injury, highlighting the need to better characterize the interplay between the primary trauma responses and compensatory effects during this early time period.
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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.