ArticleJournal of neurotrauma2016
Traumatic Brain Injury Impairs Soluble N-Ethylmaleimide-Sensitive Factor Attachment Protein Receptor Complex Formation and Alters Synaptic Vesicle Distribution in the Hippocampus.
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 23 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
23 citing papers in PubMed, 31 citations in OpenAlex.
- Type I interferon signaling in microglia drives synaptic engulfment and neuronal loss following traumatic brain injury.Research square · 2026Article
- Traumatic Brain Injury and Endocytosis: Reduced Rodent Hippocampal Endocytosis Proteins and Human Clathrin Light Chain Polymorphisms Are Associated with Impaired Neurological Outcomes After TBI.Molecular neurobiology · 2026Article
- Assessment of Neurobehavioral Performance and Markers of Synaptic Vesicle Trafficking in an Alpha-Synuclein Knockout Mouse Model after Controlled Cortical Impact Injury.Neurotrauma reports · 2025Article
- Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury.Brain and behavior · 2024Review
- Impact of dietary changes on retinal neuronal plasticity in rodent models of physical and psychological trauma.Frontiers in genetics · 2024Article
- Rapamycin Affects the Hippocampal SNARE Complex to Alleviate Cognitive Dysfunction Induced by Surgery in Aged Rats.Brain sciences · 2023Article
- Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2022Review
- Reductions in Synaptic Vesicle Glycoprotein 2 Isoforms in the Cortex and Hippocampus in a Rat Model of Traumatic Brain Injury.Molecular neurobiology · 2021Article
- Axonopathy precedes cell death in ocular damage mediated by blast exposure.Scientific reports · 2021Article
- Distinct and dementia-related synaptopathy in the hippocampus after military blast exposures.Brain pathology (Zurich, Switzerland) · 2021Article
- Exo70 intracellular redistribution after repeated mild traumatic brain injury.Biological research · 2021Article
- Differential Regional Responses in Soluble Monomeric Alpha Synuclein Abundance Following Traumatic Brain Injury.Molecular neurobiology · 2021Article
- Development and Application of 3D Bioprinted Scaffolds Supporting Induced Pluripotent Stem Cells.BioMed research international · 2021Review
- Neurogranin Protein Expression Is Reduced after Controlled Cortical Impact in Rats.Journal of neurotrauma · 2020Article
- Lithium Improves Dopamine Neurotransmission and Increases Dopaminergic Protein Abundance in the Striatum after Traumatic Brain Injury.Journal of neurotrauma · 2018Article
- Nutrient limitation affects presynaptic structures through dissociable Bassoon autophagic degradation and impaired vesicle release.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Expression profile of plasma microRNAs and their roles in diagnosis of mild to severe traumatic brain injury.PloS one · 2018Article
- Lithium increases hippocampal SNARE protein abundance after traumatic brain injury.Experimental neurology · 2017Article
- Lateral Fluid Percussion Injury Impairs Hippocampal Synaptic Soluble N-Ethylmaleimide Sensitive Factor Attachment Protein Receptor Complex Formation.Frontiers in neurology · 2017Article
- Therapeutic Potentials of Synapses after Traumatic Brain Injury: A Comprehensive Review.Neural plasticity · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) impairs neuronal function and can culminate in lasting cognitive impairment. While impaired neurotransmitter release has been well established after experimental TBI, little is understood about the mechanisms underlying this consequence. In the synapse, vesicular docking and neurotransmitter release requires the formation of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. Impairments in vesicle docking, and alterations in SNARE complex formation are associated with impaired neurotransmitter release. We hypothesized that TBI reduces SNARE complex formation and disrupts synaptic vesicle distribution in the hippocampus. To examine the effect of TBI on the SNARE complex, rats were subjected to controlled cortical impact (CCI) or sham injury, and the brains were assessed at 6 h, 1 d, one week, two weeks, or four weeks post-injury. Immunoblotting of hippocampal homogenates revealed significantly reduced SNARE complex formation at one week and two weeks post-injury. To assess synaptic vesicles distribution, rats received CCI or sham injury and the brains were processed for transmission electron microscopy at one week post-injury. Synapses in the hippocampus were imaged at 100k magnification, and vesicle distribution was assessed in pre-synaptic terminals at the active zone. CCI resulted in a significant reduction in vesicle number within 150 nm of the active zone. These findings provide the first evidence of TBI-induced impairments in synaptic vesicle docking, and suggest that reductions in the pool of readily releasable vesicles and impaired SNARE complex formation are two novel mechanisms contributing to impaired neurotransmission after TBI.
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