ArticleBrain research2014
Selective vasopressin-1a receptor antagonist prevents brain edema, reduces astrocytic cell swelling and GFAP, V1aR and AQP4 expression after focal traumatic brain injury.
Article in Brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- The Relationship Between Inflammation and the Development of Cerebral Ischaemia and Hypoxia in Traumatic Brain Injury-A Narrative Review.International journal of molecular sciences · 2025Review
- Relcovaptan: a promising therapeutic agent in traumatic spinal cord injury that acts by modulating newly identified transcriptional regulators of aquaporins compared to tolvaptan.Turkish journal of medical sciences · 2025Article
- Role of aquaporins in brain water transport and edema.Frontiers in neuroscience · 2025Review
- Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024Review
- Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?Biology · 2023Review
- The Role of Arginine-Vasopressin in Stroke and the Potential Use of Arginine-Vasopressin Type 1 Receptor Antagonists in Stroke Therapy: A Narrative Review.International journal of molecular sciences · 2023Review
- Real-time imaging of inflammation and its resolution: It's apparent because it's transparent.Immunological reviews · 2022Review
- Emerging therapeutic targets for cerebral edema.Expert opinion on therapeutic targets · 2021Review
- Astroglial Regulation of Magnocellular Neuroendocrine Cell Activities in the Supraoptic Nucleus.Neurochemical research · 2021Review
- Omega-3 Fatty Acids and Vitamin D Decrease Plasma T-Tau, GFAP, and UCH-L1 in Experimental Traumatic Brain Injury.Frontiers in nutrition · 2021Article
- Neurobiological aspects of pain in the context of alcohol use disorder.International review of neurobiology · 2021Article
- Review
- Evidence of early vasogenic edema following minor head impact that can be reduced with a vasopressin V1a receptor antagonist.Brain research bulletin · 2020Article
- Drug development in targeting ion channels for brain edema.Acta pharmacologica Sinica · 2020Article
- Establishing GPCR Targets of hMAO Active Anthraquinones fromACS omega · 2020Article
- Cerebral Edema in Traumatic Brain Injury: a Historical Framework for Current Therapy.Current treatment options in neurology · 2020Article
- Emerging Pharmacological Treatments for Cerebral Edema: Evidence from Clinical Studies.Annual review of pharmacology and toxicology · 2020Review
- Pathophysiology and treatment of cerebral edema in traumatic brain injury.Neuropharmacology · 2019Review
- Immunohistochemical Evaluation of Aquaporin-4 and its Correlation with CD68, IBA-1, HIF-1α, GFAP, and CD15 Expressions in Fatal Traumatic Brain Injury.International journal of molecular sciences · 2018Article
- Glibenclamide Produces Region-Dependent Effects on Cerebral Edema in a Combined Injury Model of Traumatic Brain Injury and Hemorrhagic Shock in Mice.Journal of neurotrauma · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
A secondary and often lethal consequence of traumatic brain injury is cellular edema that we posit is due to astrocytic swelling caused by transmembrane water fluxes augmented by vasopressin-regulated aquaporin-4 (AQP4). We therefore tested whether vasopressin 1a receptor (V1aR) inhibition would suppress astrocyte AQP4, reduce astrocytic edema, and thereby diminish TBI-induced edematous changes. V1aR inhibition by SR49059 significantly reduced brain edema after cortical contusion injury (CCI) in rat 5h post-injury. Injured-hemisphere brain water content (n=6 animals/group) and astrocytic area (n=3/group) were significantly higher in CCI-vehicle (80.5±0.3%; 18.0±1.4 µm(2)) versus sham groups (78.3±0.1%; 9.5±0.9 µm(2)), and SR49059 blunted CCI-induced increases in brain edema (79.0±0.2%; 9.4±0.8µm(2)). CCI significantly up-regulated GFAP, V1aR and AQP4 protein levels and SR49059 suppressed injury induced up regulation (n=6/group). In CCI-vehicle, sham and CCI-SR49059 groups, GFAP was 1.58±0.04, 0.47±0.02, and 0.81±0.03, respectively; V1aR was 1.00±0.06, 0.45±0.05, and 0.46±0.09; and AQP4 was 2.03±0.34, 0.49±0.04, and 0.92±0.22. Confocal immunohistochemistry gave analogous results. In CCI-vehicle, sham and CCI-SR49059 groups, fluorescence intensity of GFAP was 349±38, 56±5, and 244±30, respectively, V1aR was 601±71, 117.8±14, and 390±76, and AQP4 was 818±117, 158±5, and 458±55 (n=3/group). The results support that edema was predominantly cellular following CCI and documented that V1aR inhibition with SR49059 suppressed injury-induced up regulation of GFAP, V1A and AQP4, blunting edematous changes. Our findings suggest V1aR inhibitors may be potential therapeutic tools to prevent cellular swelling and provide treatment for post-traumatic brain edema.
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