NMDA receptor mediated phosphorylation of GluR1 subunits contributes to the appearance of calcium-permeable AMPA receptors after mechanical stretch injury
Open accessAbstract
Alterations in neuronal cytosolic calcium is a key mediator of the traumatic brain injury (TBI) pathobiology, but less is known of the role and source of calcium in shaping early changes in synaptic receptors and neural circuits after TBI. In this study, we examined the calcium source and potential phosphorylation events leading to insertion of calcium-permeable AMPARs (CP-AMPARs) after in vitro traumatic brain injury, a receptor subtype that influences neural circuit dynamics for hours to days following injury. We found that both synaptic and NR2B-containing NMDARs contribute significantly to the calcium influx following stretch injury. Moreover, an early and sustained phosphorylation of the S-831 site of the GluR1 subunit appeared after mechanical injury, and this phosphorylation was blocked with the inhibition of either synaptic NMDARs or NR2B-containing NMDARs. In comparison, mechanical injury led to no significant change in the S-845 phosphorylation of the GluR1 subunit. Although no change in S-845 phosphorylation appeared in injured cultures, we observed that inhibition of NR2B-containing NMDARs significantly increased S-845 phosphorylation 1h after injury while blockade of synaptic NMDARs did not change S-845 phosphorylation at any time point following injury. These findings show that a broad class of NMDARs are activated in parallel and that targeting either subpopulation will reverse some of the consequences of mechanical injury, providing distinct paths to treat the effects of mechanical injury on neural circuits after TBI.
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NMDAR activation is inversely related to GluA1 S845 phosphorylation, with NMDA dose-dependently reducing expression in hippocampal slices, consistent with ketamine antagonism.
“Further, NMDAR activation is inversely correlated with GluA1 S845 phosphorylation, with NMDA dose-dependently reducing expression in hippocampal slices, which is consistent with the effects of ketamine antagonism”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Spaethling et al., 2012
The Discussion (page not provided) suggests that activation of NR2A-containing NMDARs enhances S-845 phosphorylation, contrary to the claimed inverse relationship. It describes only a modest, nonsignificant decrease when a smaller extrasynaptic receptor population was activated. The cited passages do not report a dose-dependent NMDA effect in hippocampal slices or a ketamine experiment. (LLM, conf=0.88)
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- Authors
- Spaethling, J., Le, L., & Meaney, D. F.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Meaney, David F.
- ORCID
- Meaney, David F.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 46
- Issue
- 3
- Pages
- 646-654
- ISSN
- 0969-9961 (ISSN-L)
- PMC
- PMC4946953
- OpenAlex
- W2075141815
- Cited by
- 36
- References
- 60
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 3 · 2015: 6 · 2014: 1 · 2013: 4
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Public Health Service (NICHD 41699)
- National Institute of Neurological Disorders and Stroke (NS35712, R01NS035712)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD041699)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, calcium-permeable AMPA receptors, NMDA receptor, synaptic NMDA receptors, calcium influx, neural circuit dynamics
- MeSH terms
- Animals, Bicuculline, Brain Injuries, Calcium, Cells, Cultured, Phenols, Phosphorylation, Piperidines, Blotting, Western, Receptors, N-Methyl-D-Aspartate, Dizocilpine Maleate, Cell Death, Receptors, AMPA, Excitatory Amino Acid Antagonists, GABA Antagonists, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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