CXCR4-activated astrocyte glutamate release via TNFα: amplification by microglia triggers neurotoxicity

By P. Bezzi, M. Domercq, L. Brambilla, R. Galli, D. Schols, E. Clercq, A. Vescovi, G. Bagetta, G. Kollias, J. Meldolesi and 1 more. Nature Neuroscience, 2001

1,068 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Oncology

View Paper: https://www.semanticscholar.org/paper/933a5aeb28e25ceb6d513e685d42ffca543d391c

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Citations in the corpus

The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “Interestingly , glutamate release appears to follow the activation of the CXCR4 by the chemokine stromal cell-derived factor 1 (SDF-1) and is followed by rapid release of TNF-a by the microglia, which can lead to neuronal death by apoptosis (Bezzi et al., 2001).”
Tumor Necrosis Factor Alpha: A Link between Neuroinflammation and Excitotoxicity (2014, positive): “In astroglia, the interaction of TNF-α with TNFR1 initiates a sequence of intracellular signaling events that leads to generation of prostaglandin E 2 that, in turn, activates the elevation of intracellular calcium followed by glutamate exocytosis [77, 78].”
A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “Several lines of evidence suggest that all of these factors can contribute to neuronal dysfunction and cell death, either alone or in concert [40–42].”
Astrocyte roles in traumatic brain injury (2015, background): “Activated microglia also release the chemokine stromal cell-derived factor 1, which binds its receptor, CXCR4 on astrocyte to elicit even further TNFα secretion into the (peri)synaptic space (Bezzi et al., 2001).”
Inflammatory processes in Alzheimer's disease. (2007, positive): “Several lines of evidence suggest that all of these factors can contribute to neuronal dysfunction and cell death, either alone or in concert (Abbas et al., 2002; Bezzi et al., 2001; Brown and BalPrice, 2003).”
Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, positive): “A related pathway to pathology in inflammation-induced effects on behavior includes the capacity of cytokines and inflammatory mediators to increase glutamate release and decrease the expression of glutamate transporters on relevant glial elements, thereby decreasing glutamate reuptake (68,71,75,79,”
Innate immunity in the central nervous system. (2012, positive): “This cytokine, at high concentrations, impairs the capacity of astrocytes to detoxify glutamate, resulting in neuronal loss through a mechanism termed “excitotoxicity” (79, 90, 91).”
Role of Microglia in Central Nervous System Infections (2004, background): “with astrocytes, neurons, and monocytes may regulate this secretion (38, 205).”