Cited by 386Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsGenetics and Neurodevelopmental Disorders

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

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Kim, Chong-Hyun, Lisman, John E.·1999·The Journal of Neuroscience

Abstract

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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Crossref · 10.1523/jneurosci.19-11-04314.1999

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  • Interfering with actin polymerization blocks both sLTP and LTP.

    “Interfering with actin polymerization blocks both sLTP (247) as well as LTP (310).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [310]

    Citation 310 supports the LTP portion of the sentence, not the separately cited sLTP portion. In “LTP induction is inhibited by actin polymerization inhibitors” (page unavailable), the paper reports that latrunculin B reduced potentiation rather than completely blocking LTP, so “blocks” overstates its finding. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Blocking actin remodeling blocks both sLTP and LTP.

    “However, blocking actin remodeling blocks both sLTP (247) and LTP (310).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [310]

    Citation 310 is attached to the LTP portion of the sentence; the separate sLTP citation is not assessed here. In “LTP induction is inhibited by actin polymerization inhibitors” (page unavailable), latrunculin B reduced LTP, but potentiation remained at 113% versus 160% in controls. The source supports inhibition of LTP, not its complete blockade. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Actin polymerization is an essential step of LTP-stabilizing processes.

    “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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Authors
Kim, C.-H., & Lisman, J. E.
Affiliations
Brandeis University (US)
Venue
The Journal of Neuroscience
Published
1999-06-01
Volume
19
Issue
11
Pages
4314-4324
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
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
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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