ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2013
Downregulation of Src-kinase and glutamate-receptor phosphorylation after traumatic brain injury.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- How muscle talks to brain: apelin protein mediates exercise-induced antidepressant effects.Molecular psychiatry · 2026Article
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Bibliometric analysis and core target identification of network pharmacology on neuroinflammation in central nervous system disorders: Trends, collaborations, and future directions.Neuroprotection (Chichester, England) · 2025Review
- Exo70 Protects Against Memory and Synaptic Impairments Following Mild Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2025Article
- Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury.Neural regeneration research · 2023Article
- Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2022Review
- Article
- Exo70 intracellular redistribution after repeated mild traumatic brain injury.Biological research · 2021Article
- Blood-Based Glutamate Scavengers Reverse Traumatic Brain Injury-Induced Synaptic Plasticity Disruption by Decreasing Glutamate Level in Hippocampus Interstitial Fluid, but Not Cerebral Spinal Fluid, In Vivo.Neurotoxicity research · 2019Article
- Review
- Diurnal variation of NMDA receptor expression in the rat cerebral cortex is associated with traumatic brain injury damage.BMC research notes · 2018Article
- From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- Pycnogenol protects CA3-CA1 synaptic function in a rat model of traumatic brain injury.Experimental neurology · 2016Article
- Src Family Kinases in Brain Edema After Acute Brain Injury.Acta neurochirurgica. Supplement · 2016Article
- Glutamate and GABA imbalance following traumatic brain injury.Current neurology and neuroscience reports · 2015Review
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7 authors.
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Abstract
Phosphorylation of N-methyl-D-aspartate (NMDA) receptors is a major regulatory mechanism underlying synaptic plasticity. However, changes in NMDA receptors and phosphorylation after traumatic brain injury (TBI) remain incompletely understood. Using an animal TBI model, we observed that the protein level of NMDA receptor subunit NR2B was downregulated in synaptosomal fractions obtained from the ipsilateral neocortical injury region, whereas the levels of NR2A, NR1, and PSD93 were not significantly altered at 4 and 24 hours after TBI. Further investigation showed that tyrosine phosphorylations of NR2B Y1472 and PSD93 Y340 in synaptosomal fractions were significantly decreased relative to their total protein level after TBI. Correspondingly, phosphorylation of the Src-kinase-inhibitory site Y527 was increased, whereas phosphorylation of the activation site Y416 was decreased, indicating that the activity of Src kinase is significantly inhibited after TBI. In comparison, other Src family kinase substrates of NMDA receptor, NR2A Y1246, NR2A Y1325, and NR2B Y1070 were not obviously affected after TBI. The results suggest that TBI downregulates the Src-kinase-mediated phosphorylation of NR2 and PSD93 to destabilize the synaptic localization of NMDA receptors. Therefore, post-TBI loss of NMDA receptors may contribute to the depression of synaptic activity after TBI.
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