ArticleJournal of neurotrauma2008
Inhibition of NR2B phosphorylation restores alterations in NMDA receptor expression and improves functional recovery following traumatic brain injury in mice.
Article in Journal of neurotrauma, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- The link between impact-induced tensile strain and dendritic spine morphology in porcine brain tissue.PloS one · 2025Article
- Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model.Behavioural brain research · 2023Article
- Neonatal microglia and proteinase inhibitors-treated adult microglia improve traumatic brain injury in rats by resolving the neuroinflammation.Bioengineering & translational medicine · 2022Article
- MicroRNA-124/Death-Associated Protein Kinase 1 Signaling Regulates Neuronal Apoptosis in Traumatic Brain InjuryFrontiers in cellular neuroscience · 2022Article
- Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2022Review
- Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury.Journal of neurotrauma · 2021Article
- Hyperhomocysteinemia is an emerging comorbidity in ischemic stroke.Experimental neurology · 2021Review
- The Emergence of Model Systems to Investigate the Link Between Traumatic Brain Injury and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Microglia dynamics in adolescent traumatic brain injury.Journal of neuroinflammation · 2020Review
- Oligomer β-amyloid Induces Hyperactivation of Ras to Impede NMDA Receptor-Dependent Long-Term Potentiation in Hippocampal CA1 of Mice.Frontiers in pharmacology · 2020Article
- Traumatic Brain Injury-Induced Sex-Dependent Changes in Late-Onset Sensory Hypersensitivity and Glutamate Neurotransmission.Frontiers in neurology · 2020Article
- Bridging the gap: Mechanisms of plasticity and repair after pediatric TBI.Experimental neurology · 2019Review
- Hyperhomocysteinemia leads to exacerbation of ischemic brain damage: Role of GluN2A NMDA receptors.Neurobiology of disease · 2019Article
- Mild Blast Injury Produces Acute Changes in Basal Intracellular Calcium Levels and Activity Patterns in Mouse Hippocampal Neurons.Journal of neurotrauma · 2018Article
- Huperzine A alleviates neuroinflammation, oxidative stress and improves cognitive function after repetitive traumatic brain injury.Metabolic brain disease · 2017Article
- Environmental Enrichment Mitigates Deficits after Repetitive Mild Traumatic Brain Injury.Journal of neurotrauma · 2017Article
- Antagonistic action on NMDA/GluN2B mediated currents of two peptides that were conantokin-G structure-based designed.BMC neuroscience · 2017Article
- D-Cycloserine Restores Experience-Dependent Neuroplasticity after Traumatic Brain Injury in the Developing Rat Brain.Journal of neurotrauma · 2017Article
- The AMPAR Antagonist Perampanel Attenuates Traumatic Brain Injury Through Anti-Oxidative and Anti-Inflammatory Activity.Cellular and molecular neurobiology · 2017Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) triggers a massive glutamate efflux, hyperactivation of N-methyl-D-aspartate receptors (NMDARs) and neuronal cell death. Previously it was demonstrated that, 15 min following experimentally induced closed head injury (CHI), the density of activated NMDARs increases in the hippocampus, and decreases in the cortex at the impact site. Here we show that CHI-induced alterations in activated NMDARs correlate with changes in the expression levels of the major NMDARs subunits. In the hippocampus, the expression of NR1, NR2A, and NR2B subunits as well as the GluR1 subunit of the AMPA receptor (AMPAR) were increased, while in the cortex at the impact site, we found a decrease in the expression of these subunits. We demonstrate that CHI-induced increase in the expression of NMDAR subunits and GluR1 in the hippocampus, but not in the cortex, is associated with an increase in NR2B tyrosine phosphorylation. Furthermore, inhibition of NR2B-phosphorylation by the tyrosine kinase inhibitor PP2 restores the expression of this subunit to its normal levels. Finally, a single injection of PP2, prior to the induction of CHI, resulted in a significant improvement in long-term recovery of motor functions observed in CHI mice. These results provide a new mechanism by which acute trauma contributes to the development of secondary damage and functional deficits in the brain, and suggests a possible role for Src tyrosine kinase inhibitors as preoperative therapy for planned neurosurgical procedures.
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