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A Role of Actin Filament in Synaptic Transmission and Long-Term Potentiation
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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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