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A Role of Actin Filament in Synaptic Transmission and Long-Term Potentiation
Open accessAbstract
The role of actin filaments in synaptic function has been studied in the CA1 region of the rat hippocampal slice. Bath application (2 hr) of the actin polymerization inhibitor latrunculin B did not substantially affect the shape of dendrites or spines. However, this and other drugs that affect actin did affect synaptic function. Bath-applied latrunculin B reduced the synaptic response. Several lines of evidence indicate that a component of this effect is presynaptic. To specifically test for a postsynaptic role for actin, latrunculin B or phalloidin, an actin filament stabilizer, was perfused into the postsynaptic neuron. The magnitude of long-term potentiation (LTP) was decreased at times when baseline transmission was not yet affected. Longer applications produced a decrease in baseline AMPA receptor (AMPAR)-mediated transmission. The magnitude of the NMDA receptor-mediated transmission was unaffected, indicating a specific effect on the AMPAR. These results suggest that postsynaptic actin filaments are involved in a dynamic process required to maintain AMPAR-mediated transmission and to enhance it during LTP.
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“Interfering with actin polymerization blocks both sLTP (247) as well as LTP (310).”
From Synaptic memory and CaMKII (2023) · cites this paper as [310]
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“However, blocking actin remodeling blocks both sLTP (247) and LTP (310).”
From Synaptic memory and CaMKII (2023) · cites this paper as [310]
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“The expression of AMPA receptors in spines is dependent on F-actin11,17 and scaffolding proteins18,19.”
From Structural basis of long-term potentiation in single dendritic spines (2004) · cites this paper as [17]
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“Actin polymerization is an essential step of this kind (9, 15–17)”
From Synaptic evidence for the efficacy of spaced learning (2012) · cites this paper as [15]
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Metadata
- Authors
- Kim, C.-H., & Lisman, J. E.
- Affiliations
- Brandeis University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1999-06-01
- Volume
- 19
- Issue
- 11
- Pages
- 4314-4324
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6782630
- OpenAlex
- W2110065479
- Cited by
- 386
- References
- 47
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 14 · 2020: 10 · 2019: 4 · 2018: 4 · 2017: 10 · 2016: 12 · 2015: 8 · 2014: 15 · 2013: 10 · 2012: 22
- FWCI
- 7.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- W. M. Keck Foundation
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS027337, 5 RO1 NS27337-09)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- F-actin, synaptic transmission, long-term potentiation, latrunculin B, phalloidin, AMPA receptors, NMDA receptor, dendritic spines, hippocampal CA1, actin polymerization
- MeSH terms
- Actins, Animals, Synaptic Transmission, Phalloidine, Protein Synthesis Inhibitors, Thiazoles, Cytochalasin D, Long-Term Potentiation, Bridged Bicyclo Compounds, Heterocyclic, Rats, Long-Evans, Rats, Thiazolidines, In Vitro Techniques
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