Stimulation of Microglial Metabotropic Glutamate Receptor mGlu2 Triggers Tumor Necrosis Factor α-Induced Neurotoxicity in Concert with Microglial-Derived Fas Ligand
Open accessAbstract
Activated microglia may be detrimental to neuronal survival in a number of neurodegenerative diseases. Thus, strategies that reduce microglial neurotoxicity may have therapeutic benefit. Stimulation of group II metabotropic glutamate (mGlu) receptors on rat primary microglia with the specific group II agonist 2S,2′R,3′R-2-(2′,3′-dicarboxy-cyclopropyl)glycine for 24 h induced microglial activation and resulted in a neurotoxic microglial phenotype. These effects were attributable to preferential mGlu2 stimulation, becauseN-acetyl-l-aspartyl-l-glutamate, a specific mGlu3 agonist, did not induce microglial activation or neurotoxicity. Stimulation of microglial mGlu2 but not mGlu3 induced caspase-3 activation in cerebellar granule neurons in culture, using microglial-conditioned media as well as cocultures. Stimulation of microglial mGlu2 induced tumor necrosis factor-α (TNFα) release, which contributed to microglial neurotoxicity mediated via neuronal TNF receptor 1 and caspase-3 activation. Stimulation of microglial group I or III mGlu receptors did not induce TNFα release. TNFα was only neurotoxic in the presence of microglia or microglial-conditioned medium. The toxicity of TNFα could be prevented by coexposure of neurons to conditioned medium from microglia stimulated by the specific group III agonistl-2-amino-4-phosphono-butyric acid. The neurotoxicity of TNFα derived from mGlu2-stimulated microglia was potentiated by microglial-derived Fas ligand (FasL), the death receptor ligand. FasL was constitutively expressed in microglia and shed after mGlu2 stimulation. Our data suggest that selective and inverse modulation of microglial mGlu2 and mGlu3 may prove a therapeutic target in neuroinflammatory diseases such as Alzheimer's disease and multiple sclerosis.
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TNF-α binds to TNFR1, leading to neuronal apoptosis.
“TNF-α has been reported to bind to tumor necrosis factor (TNFR1), leading to neuronal apoptosis [155,156].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [155]
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- Authors
- Taylor, D. L., Jones, F., Kubota, E. S. F. C. S., & Pocock, J. M.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- Corresponding author
- Pocock, Jennifer M.
- ORCID
- Pocock, Jennifer M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-03-16
- Volume
- 25
- Issue
- 11
- Pages
- 2952-2964
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1991288075
- Cited by
- 308
- References
- 66
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 10 · 2023: 13 · 2022: 12 · 2021: 23 · 2020: 16 · 2019: 8 · 2018: 14 · 2017: 11 · 2016: 13 · 2015: 24 · 2014: 17 · 2013: 15 · 2012: 15
- FWCI
- 9.29
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- microglial activation, mGlu2 receptor, mGlu3 receptor, group II metabotropic glutamate receptors, TNF-α, neurotoxicity, Fas ligand, caspase-3, TNF receptor 1, cerebellar granule cells, neuroinflammation, Alzheimer's disease, multiple sclerosis
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