The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Preconditioning Doses of NMDA Promote Neuroprotection by Enhancing Neuronal Excitability
Open accessAbstract
Neuroprotection can be induced by low doses of NMDA, which activate both synaptic and extrasynaptic NMDA receptors. This is in apparent contradiction with our recent findings that extrasynaptic NMDA receptor signaling exerts a dominant inhibitory effect on prosurvival signaling from synaptic NMDA receptors. Here we report that exposure to low preconditioning doses of NMDA results in preferential activation of synaptic NMDA receptors because of a dramatic increase in action potential firing. Both acute and long-lasting phases of neuroprotection in the face of apoptotic or excitotoxic insults are dependent on this firing enhancement. Key mediators of synaptic NMDA receptor-dependent neuroprotection, phosphatidylinositol 3 kinase-Akt (PI3 kinase-Akt) signaling to Forkhead box subgroup O (FOXO) export and glycogen synthase kinase 3β (GSK3β) inhibition and cAMP response element-binding protein-dependent (CREB-dependent) activation of brain-derived neurotrophic factor (BDNF), can be induced only by low doses of NMDA via this action potential-dependent route. In contrast, NMDA doses on the other side of the toxicity threshold do not favor synaptic NMDA receptor activation because they strongly suppress firing rates below baseline. The classic bell-shaped curve depicting neuronal fate in response to NMDA dose can be viewed as the net effect of two antagonizing (synaptic vs extrasynaptic) curves: via increased firing the synaptic signaling dominates at low doses, whereas firing becomes suppressed and extrasynaptic signaling dominates as the toxicity threshold is crossed.
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Cites
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Blockade of NMDA Receptors and Apoptotic Neurodegeneration in the Developing Brain
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Self-citationCa2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism
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Cited by
Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders
Hardingham, G. E., & Bading, H. (2010) · Nature Reviews Neuroscience · doi:10.1038/nrn2911 · Cited by 1,644
Self-citationFunctional Repression of cAMP Response Element in 6-Hydroxydopamine-treated Neuronal Cells
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Excitotoxicity and stroke: Identifying novel targets for neuroprotection
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Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions
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Metadata
- Authors
- Soriano, F. X., Papadia, S., Hofmann, F., Hardingham, N. R., Bading, H., & Hardingham, G. E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2006-04-26
- Volume
- 26
- Issue
- 17
- Pages
- 4509-4518
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2141750111
- Cited by
- 235
- References
- 10
- FWCI
- 8.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Soriano, F. X., Papadia, S., Hofmann, F., Hardingham, N. R., Bading, H., & Hardingham, G. E. (2006). Preconditioning Doses of NMDA Promote Neuroprotection by Enhancing Neuronal Excitability. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0455-06.2006
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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