The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Soluble Aβ Oligomers Inhibit Long-Term Potentiation through a Mechanism Involving Excessive Activation of Extrasynaptic NR2B-Containing NMDA Receptors
Open accessAbstract
In Alzheimer's disease (AD), dementia severity correlates strongly with decreased synapse density in hippocampus and cortex. Numerous studies report that hippocampal long-term potentiation (LTP) can be inhibited by soluble oligomers of amyloid β-protein (Aβ), but the synaptic elements that mediate this effect remain unclear. We examined field EPSPs and whole-cell recordings in wild-type mouse hippocampal slices. Soluble Aβ oligomers from three distinct sources (cultured cells, AD cortex, or synthetic peptide) inhibited LTP, and this was prevented by the selective NR2B inhibitors ifenprodil and Ro 25-6981. Soluble Aβ enhanced NR2B-mediated NMDA currents and extrasynaptic responses; these effects were mimicked by the glutamate reuptake inhibitor dl -threo-β-benzyloxyaspartic acid. Downstream, an Aβ-mediated rise in p38 mitogen-activated protein kinase (MAPK) activation was followed by downregulation of cAMP response element-binding protein, and LTP impairment was prevented by inhibitors of p38 MAPK or calpain. Thus, soluble Aβ oligomers at low nanomolar levels present in AD brain increase activation of extrasynaptic NR2B-containing receptors, thereby impairing synaptic plasticity.
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Self-citationDiffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
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Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
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Self-citationRegulation of NMDA receptor trafficking by amyloid-β
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“The depressed synaptic NR2B proteins we observed at 6 h could be explained by endocytosis of surface NMDAR (Snyder et al., 2005) associated with A - mediated effects of excess glutamate levels (Vaslin et al., 2007).”
BackgroundResultAβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease
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Amyloid β protein immunotherapy neutralizes Aβ oligomers that disrupt synaptic plasticity in vivo
Klyubin, I., Walsh, D. M., Lemere, C. A., Cullen, W. K., Shankar, G. M., Betts, V., Spooner, E. T., Jiang, L., Anwyl, R., Selkoe, D. J., et al. (2005) · Nature Medicine · doi:10.1038/nm1234 · Cited by 489
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NMDA receptor subunit diversity: impact on receptor properties, synaptic plasticity and disease
Paoletti, P., Bellone, C., & Zhou, Q. (2013) · Nature Reviews Neuroscience · doi:10.1038/nrn3504 · Cited by 2,523
Alzheimer Mechanisms and Therapeutic Strategies
Huang, Y., & Mucke, L. (2012) · Cell · doi:10.1016/j.cell.2012.02.040 · Cited by 1,758
Fricker, M., Tolkovsky, A. M., Borutaite, V., Coleman, M., & Brown, G. C. (2018) · Physiological Reviews · doi:10.1152/physrev.00011.2017 · Cited by 1,108
Network abnormalities and interneuron dysfunction in Alzheimer disease
Palop, J. J., & Mucke, L. (2016) · Nature reviews. Neuroscience · doi:10.1038/nrn.2016.141 · Cited by 1,022
Neurotoxicity of Amyloid -Protein: Synaptic and Network Dysfunction
Mucke, L., & Selkoe, D. J. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006338 · Cited by 1,000
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Metadata
- Authors
- Li, S., Jin, M., Koeglsperger, T., Shepardson, N. E., Shankar, G. M., & Selkoe, D. J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-05-04
- Volume
- 31
- Issue
- 18
- Pages
- 6627-6638
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2028174194
- Cited by
- 671
- References
- 16
- FWCI
- 15.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Li, S., Jin, M., Koeglsperger, T., Shepardson, N. E., Shankar, G. M., & Selkoe, D. J. (2011). Soluble Aβ Oligomers Inhibit Long-Term Potentiation through a Mechanism Involving Excessive Activation of Extrasynaptic NR2B-Containing NMDA Receptors. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0203-11.2011
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
