ArticleJournal of neurotrauma2013
Activation of mGluR5 and inhibition of NADPH oxidase improves functional recovery after traumatic brain injury.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- A Systematic Review on Traumatic Brain Injury Pathophysiology and Role of Herbal Medicines in its Management.Current neuropharmacology · 2023Pooled it
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- Long-term potentiation and long-term depression are both impaired afterBiomedical physics & engineering express · 2025Article
- Anxiety and Depression: Triggers for Cognitive Loss, Alzheimer's Disease, and Neurodegeneration.Current neurovascular research · 2025Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- The Physio-Pathological Role of Group I Metabotropic Glutamate Receptors Expressed by Microglia in Health and Disease with a Focus on Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- The Implication of Glial Metabotropic Glutamate Receptors in Alzheimer's Disease.Current neuropharmacology · 2023Review
- The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications.Frontiers in pharmacology · 2023Review
- The Role of Neuroglial Metabotropic Glutamate Receptors in Alzheimer's Disease.Current neuropharmacology · 2023Review
- A multilayer network model of neuron-astrocyte populations in vitro reveals mGluRNetwork neuroscience (Cambridge, Mass.) · 2022Article
- ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway.Cell communication and signaling : CCS · 2022Article
- Changes in Metabotropic Glutamate Receptor Gene Expression in Rat Brain in a Lithium-Pilocarpine Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2022Article
- Article
- Targeting the Type 5 Metabotropic Glutamate Receptor: A Potential Therapeutic Strategy for Neurodegenerative Diseases?Frontiers in pharmacology · 2022Review
- Therapeutic targeting of microglia mediated oxidative stress after neurotrauma.Frontiers in medicine · 2022Review
- Enhanced Akt/GSK-3β/CREB signaling mediates the anti-inflammatory actions of mGluR5 positive allosteric modulators in microglia and following traumatic brain injury in male mice.Journal of neurochemistry · 2021Article
- Modulating neuroinflammation and oxidative stress to prevent epilepsy and improve outcomes after traumatic brain injury.Neuropharmacology · 2020Review
- Dementia, Depression, and Associated Brain Inflammatory Mechanisms after Spinal Cord Injury.Cells · 2020Review
- Microglial Depletion with CSF1R Inhibitor During Chronic Phase of Experimental Traumatic Brain Injury Reduces Neurodegeneration and Neurological Deficits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- NADExperimental neurology · 2020Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Abstract Traumatic brain injury (TBI) induces microglial activation, which can contribute to secondary tissue loss. Activation of mGluR5 reduces microglial activation and inhibits microglial-mediated neurodegeneration in vitro, and is neuroprotective in experimental models of CNS injury. In vitro studies also suggest that the beneficial effects of mGluR5 activation involve nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibition in activated microglia. We hypothesized that activation of mGluR5 by the selective agonist CHPG after TBI in mice is neuroprotective and that its therapeutic actions are mediated by NADPH oxidase inhibition. Vehicle, CHPG, or CHPG plus the mGluR5 antagonist (MPEP), were administered centrally, 30 minutes post-TBI, and functional recovery and lesion volume was assessed. CHPG significantly attenuated post-traumatic sensorimotor and cognitive deficits, and reduced lesion volumes; these effects were blocked by MPEP, thereby indicating neuroprotection involved selective activation of mGluR5. CHPG treatment also reduced NFκB activity and nitrite production in lipopolysaccharide-stimulated microglia and the protective effects of CHPG treatment were abrogated in NADPH oxidase deficient microglial cultures (gp91(phox-/-)). To address whether the neuroprotective effects of CHPG are mediated via the inhibition of NADPH oxidase, we administered the NADPH oxidase inhibitor apocynin with or without CHPG treatment after TBI. Both apocynin or CHPG treatment alone improved sensorimotor deficits and reduced lesion volumes when compared with vehicle-treated mice; however, the combined CHPG + apocynin treatment was not superior to CHPG alone. These data suggest that the neuroprotective effects of activating mGluR5 receptors after TBI are mediated, in part, via the inhibition of NADPH oxidase.
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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.