Interleukin-1β Enhances NMDA Receptor-Mediated Intracellular Calcium Increase through Activation of the Src Family of Kinases
By B. Viviani, S. Bartesaghi, F. Gardoni, A. Vezzani, M. Behrens, T. Bártfai, M. Binaglia, E. Corsini, M. Luca, C. Galli and 1 more. Journal of Neuroscience, 2003
846 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/2e82a0201ac85199a523fed68c982cff3832225d
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In Cellular and Molecular Neuroscience
In Immunology
In Neurology
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- Sanjay M. Sisodiya
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Citations in the corpus
- Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, background): “, 2009), high levels of IL-1 (Balosso et al., 2008; Vezzani et al., 1999; Viviani et al., 2003), or the secretion of HMGB1 (a dam-”
- Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord (2008, background): “Our data also demonstrated an enhancement of NMDA current by TNF and IL-1 , in parallel with reports showing that IL-1 increases NMDA receptor phosphorylation in the trigeminal nucleus (Guo et al., 2007) and NMDA-induced Ca2 influx in hippocampal neurons (Viviani et al., 2003).”
- The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, methodology): “Inhibitors of these proteins are able to block IL-1β-induced phosphorylation of either the NR1 subunit or NR2A/B subunit of the NMDA receptor in vitro similarly to IL-1ra (Viviani et al. 2003).”
- The role of inflammation in the development of epilepsy (2018, background): “It has been suggested that IL-1β induces seizures through the upregulation of NMDA receptors on postsynaptic cells via an activation of the GluN2B subunit of the NMDA receptor [18].”
- Drug Resistance in Epilepsy: Clinical Impact, Potential Mechanisms, and New Innovative Treatment Options (2020, background): “…induced by the activation of the IL-1bIL-1R1 axis in neurons leads to increased excitability and excitotoxicity and promotes seizures mediated by NMDA receptor subunit N2B subunit phosphorylation and enhanced neuronal Ca2+ influx through NMDA receptors (Viviani et al., 2003; Balosso et al., 2008).”
- The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “IL-1β appears to modulate glutamate receptors in hippocampal neurons, for example, IL-1β reduces AMPA-dependent excitatory post-synaptic currents, but enhances NMDA-mediated calcium influx (Viviani et al., 2003; Yang et al., 2005).”
- The role of inflammation in epilepsy (2010, positive): “140,141 Since the ceramide-activated Src system is a major modulator of ion channel activity, inhibitors of this system (acting at the cytosolic adaptor MyD88, the biosynthetic steps of ceramide, or the level of Src activity) should arrest inflammation-mediated hyperexcitability.”
- Inflammatory Cytokines in Experimental and Human Stroke (2012, background): “Several lines of evidence indicate that, at least for IL-1 and TNF, similar effects are also observed in central nervous system neurons (Viviani et al, 2003; Gardoni et al, 2011).”