The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Extracellular Alpha-Synuclein Oligomers Modulate Synaptic Transmission and Impair LTP Via NMDA-Receptor Activation
Open accessAbstract
Parkinson's disease (PD) is the most common representative of a group of disorders known as synucleinopathies, in which misfolding and aggregation of α-synuclein (a-syn) in various brain regions is the major pathological hallmark. Indeed, the motor symptoms in PD are caused by a heterogeneous degeneration of brain neurons not only in substantia nigra pars compacta but also in other extrastriatal areas of the brain. In addition to the well known motor dysfunction in PD patients, cognitive deficits and memory impairment are also an important part of the disorder, probably due to disruption of synaptic transmission and plasticity in extrastriatal areas, including the hippocampus. Here, we investigated the impact of a-syn aggregation on AMPA and NMDA receptor-mediated rat hippocampal (CA3-CA1) synaptic transmission and long-term potentiation (LTP), the neurophysiological basis for learning and memory. Our data show that prolonged exposure to a-syn oligomers, but not monomers or fibrils, increases basal synaptic transmission through NMDA receptor activation, triggering enhanced contribution of calcium-permeable AMPA receptors. Slices treated with a-syn oligomers were unable to respond with further potentiation to theta-burst stimulation, leading to impaired LTP. Prior delivery of a low-frequency train reinstated the ability to express LTP, implying that exposure to a-syn oligomers drives the increase of glutamatergic synaptic transmission, preventing further potentiation by physiological stimuli. Our novel findings provide mechanistic insight on how a-syn oligomers may trigger neuronal dysfunction and toxicity in PD and other synucleinopathies.
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α-Synuclein is phosphorylated in synucleinopathy lesions
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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
Obeso, J. A., Stamelou, M., Goetz, C. G., Poewe, W., Lang, A. E., Weintraub, D., Burn, D., Halliday, G. M., Bezard, E., Przedborski, S., et al. (2017) · Movement Disorders · doi:10.1002/mds.27115 · Cited by 859
Modeling Parkinson’s Disease With the Alpha-Synuclein Protein
Gómez-Benito, M., Granado, N., García-Sanz, P., Michel, A., Dumoulin, M., & Moratalla, R. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00356 · Cited by 437
Alpha-Synuclein Oligomers—Neurotoxic Molecules in Parkinson's Disease and Other Lewy Body Disorders
Ingelsson, M. (2016) · Frontiers in Neuroscience · doi:10.3389/fnins.2016.00408 · Cited by 344
Self-citationProtein phosphorylation in neurodegeneration: friend or foe?
Tenreiro, S., Eckermann, K., & Outeiro, T. F. (2014) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2014.00042 · Cited by 252
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Metadata
- Authors
- Diógenes, M. J., Dias, R. B., Rombo, D. M., Vicente Miranda, H., Maiolino, F., Guerreiro, P., Näsström, T., Franquelim, H. G., Oliveira, L. M. A., Castanho, M. A. R. B., Lannfelt, L., Bergström, J., Ingelsson, M., Quintas, A., Sebastião, A. M., Lopes, L. V., & Outeiro, T. F.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-08-22
- Volume
- 32
- Issue
- 34
- Pages
- 11750-11762
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2036203077
- Cited by
- 271
- References
- 59
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Diógenes, M. J., Dias, R. B., Rombo, D. M., Vicente Miranda, H., Maiolino, F., Guerreiro, P., Näsström, T., Franquelim, H. G., Oliveira, L. M. A., Castanho, M. A. R. B., Lannfelt, L., Bergström, J., Ingelsson, M., Quintas, A., Sebastião, A. M., Lopes, L. V., & Outeiro, T. F. (2012). Extracellular Alpha-Synuclein Oligomers Modulate Synaptic Transmission and Impair LTP Via NMDA-Receptor Activation. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0234-12.2012
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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.
