ArticleJournal of neurotrauma2017
Inhibition of Endocannabinoid Degradation Improves Outcomes from Mild Traumatic Brain Injury: A Mechanistic Role for Synaptic Hyperexcitability.
Article in Journal of neurotrauma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 54 citations in OpenAlex.
- Endocannabinoid Modulation in Headache: Mechanisms, Models, and Translational Therapies.Cells · 2026Review
- The effect of traumatic brain injury on learning and memory: A synaptic focus.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Mechanisms Underlying Hazardous Alcohol Use After Mild Traumatic Brain Injury.Alcohol research : current reviews · 2025Review
- Overabundant endocannabinoids in neurons are detrimental to cognitive function.bioRxiv : the preprint server for biology · 2024Article
- Aquaporin 4 and the endocannabinoid system: a potential therapeutic target in brain injury.Experimental brain research · 2024Review
- Traumatic Stress-Induced Increases in Anxiety-like Behavior and Alcohol Self-Administration Are Mediated by Central Amygdala CRF1 Neurons That Project to the Lateral Hypothalamus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Repeated Mild Traumatic Brain Injury and JZL184 Produce Sex-Specific Increases in Anxiety-Like Behavior and Alcohol Consumption in Wistar Rats.Journal of neurotrauma · 2023Article
- Article
- JZL184 increases anxiety-like behavior and does not reduce alcohol consumption in female rats after repeated mild traumatic brain injury.bioRxiv : the preprint server for biology · 2023Article
- Endocannabinoid control of neuroinflammation in traumatic brain injury by monoacylglycerol lipase in astrocytes.Neural regeneration research · 2023Article
- Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.Pharmacology & therapeutics · 2023Review
- Cannabidiol's neuroprotective properties and potential treatment of traumatic brain injuries.Frontiers in neurology · 2023Review
- Review
- 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
- Long-term increase in sensitivity to ketamine's behavioral effects in mice exposed to mild blast induced traumatic brain injury.Experimental neurology · 2022Article
- Brain Injury Effects on Neuronal Activation and Synaptic Transmission in the Basolateral Amygdala of Adult Male and Female Wistar Rats.Journal of neurotrauma · 2022Article
- Enhancing endocannabinoid signalling in astrocytes promotes recovery from traumatic brain injury.Brain : a journal of neurology · 2022Article
- Article
- Review
- Use of Medical Cannabis to Treat Traumatic Brain Injury.Journal of neurotrauma · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is an increasingly prevalent condition affecting soldiers, athletes, and motor vehicle accident victims. Unfortunately, it currently lacks effective therapeutic interventions. TBI is defined as a primary mechanical insult followed by a secondary cascade involving inflammation, apoptosis, release of reactive oxygen species, and excitotoxicity, all of which can cause synaptic changes, altered neuronal signaling, and, ultimately, behavioral changes. Previously we showed that preventing degradation of the endocannabinoid (EC) 2-acylglycerol (2-AG) with JZL184 after mild TBI attenuated neuroinflammation and improved recovery of neurobehavioral function during the early 24 h post-TBI period. The aim of this study was to extend the timeline of observations to 2 weeks post-injury and to investigate JZL184's impact on synaptic transmission, which we view as a potential mechanism for TBI-induced cellular and behavioral pathology. Adult male rats underwent mild TBI (mTBI) followed by a single intraperitoneal injection of JZL184 or vehicle 30 min post-injury. JZL184 administered-TBI animals showed improved neurobehavioral recovery compared with vehicle-injected TBI animals beginning 24 h post-injury and persisting for 2 weeks. JZL184-treated animals had significantly diminished gray and white matter astrocyte activation when compared with vehicle-treated animals at day 7 post-TBI. JZL184 administration significantly attenuated the increased pGluR1
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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.