ArticlePloS one2015
Changes in cannabinoid receptors, aquaporin 4 and vimentin expression after traumatic brain injury in adolescent male mice. Association with edema and neurological deficit.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- Promotion of recovery from Traumatic Brain Injury (TBI) by Granulocyte Colony-Stimulating Factor (G-CSF) treatment requires cannabinoid receptor type 2 activity.Journal of cannabis research · 2025Article
- Experimental study of cerebral edema and expression of VEGF and AQP4 in the penumbra area of rat brain trauma.Scientific reports · 2025Article
- The effect of traumatic brain injury on learning and memory: A synaptic focus.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Vimentin and p53 Immunoreactivity in Cases of Traumatic Brain Injury.Journal of personalized medicine · 2025Article
- Review
- CB1 Receptor Activation Provides Neuroprotection in an Animal Model of Glutamate-Induced Excitotoxicity Through a Reduction of NOX-2 Activity and Oxidative Stress.CNS neuroscience & therapeutics · 2024Article
- Aquaporin 4 and the endocannabinoid system: a potential therapeutic target in brain injury.Experimental brain research · 2024Review
- Altered endocannabinoid metabolism compromises the brain-CSF barrier and exacerbates chronic deficits after traumatic brain injury in mice.Experimental neurology · 2023Article
- Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review.Frontiers in neurology · 2023Review
- Cannabinoid CB2 Receptors in Neurodegenerative Proteinopathies: New Insights and Therapeutic Potential.Biomedicines · 2022Review
- Case studies in neuroscience: reversible signatures of edema following electric and piezoelectric craniotomy drilling in macaques.Journal of neurophysiology · 2022Article
- Recovery from Traumatic Brain Injury Following Treatment with Δ9-Tetrahydrocannabinol Is Associated with Increased Expression of Granulocyte-Colony Stimulating Factor and Other Neurotrophic Factors.Cannabis and cannabinoid research · 2022Article
- Administration of ΔCannabis and cannabinoid research · 2022Article
- A Focal Impact Model of Traumatic Brain Injury inInternational journal of molecular sciences · 2022Article
- Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target.Neurochemical research · 2022Review
- New Insights and Potential Therapeutic Targeting of CB2 Cannabinoid Receptors in CNS Disorders.International journal of molecular sciences · 2022Review
- Potential Role of Cannabinoid Type 2 Receptors in Neuropsychiatric and Neurodegenerative Disorders.Frontiers in psychiatry · 2022Review
- Chronic Anxiety- and Depression-Like Behaviors Are Associated With Glial-Driven Pathology Following Repeated Blast Induced Neurotrauma.Frontiers in behavioral neuroscience · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) incidence rises during adolescence because during this critical neurodevelopmental period some risky behaviors increase. The purpose of this study was to assess the contribution of cannabinoid receptors (CB1 and CB2), blood brain barrier proteins (AQP4) and astrogliosis markers (vimentin) to neurological deficit and brain edema formation in a TBI weight drop model in adolescent male mice. These molecules were selected since they are known to change shortly after lesion. Here we extended their study in three different timepoints after TBI, including short (24h), early mid-term (72h) and late mid-term (two weeks). Our results showed that TBI induced an increase in brain edema up to 72 h after lesion that was directly associated with neurological deficit. Neurological deficit appeared 24 h after TBI and was completely recovered two weeks after trauma. CB1 receptor expression decreased after TBI and was negatively correlated with edema formation and behavioral impairments. CB2 receptor increased after injury and was associated with high neurological deficit whereas no correlation with edema was found. AQP4 increased after TBI and was positively correlated with edema and neurological impairments as occurred with vimentin expression in the same manner. The results suggest that CB1 and CB2 differ in the mechanisms to resolve TBI and also that some of their neuroprotective effects related to the control of reactive astrogliosis may be due to the regulation of AQP4 expression on the end-feet of astrocytes.
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