Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization
Open accessAbstract
Dendritic spines are small protrusive structures on dendritic surfaces, and function as postsynaptic compartments for excitatory synapses. Plasticity of spine structure is associated with many forms of long-term neuronal plasticity, learning and memory. Inside these small dendritic compartments, biochemical states and protein-protein interactions are dynamically modulated by synaptic activity, leading to the regulation of protein synthesis and reorganization of cytoskeletal architecture. This in turn causes plasticity of structure and function of the spine. Technical advances in monitoring molecular behaviors in single dendritic spines have revealed that each signaling pathway is differently regulated across multiple spatiotemporal domains. The spatial pattern of signaling activity expands from a single spine to the nearby dendritic area, dendritic branch and the nucleus, regulating different cellular events at each spatial scale. Temporally, biochemical events are typically triggered by short Ca2+ pulses (~10-100 ms). However, these signals can then trigger activation of downstream protein cascades that can last from milliseconds to hours. Recent imaging studies provide many insights into the biochemical processes governing signaling events of molecular assemblies at different spatial localizations. Here we highlight recent findings of signaling dynamics during synaptic plasticity and discuss their roles in long-term structural plasticity of dendritic spines.
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The strongest case for the requirement of downstream CaMKII targets in sLTP, and likely LTP, is the actin cytoskeleton.
“In summary, perhaps the strongest case for the requirement of downstream CaMKII targets in sLTP, and likely LTP, is the actin cytoskeleton (30, 313, 321)”
From Synaptic memory and CaMKII (2023) · cites this paper as [321]
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“In summary, perhaps the strongest case for the requirement of downstream CaMKII targets in sLTP, and likely LTP, is the actin cytoskeleton (30, 313, 321), although the need for phosphorylation of downstream targets is debated (see sect.”
Background
- Authors
- Nakahata, Y., & Yasuda, R.
- Affiliations
- Max Planck Florida Institute for Neuroscience (US)
- Corresponding author
- Yasuda, Ryohei
- Venue
- Frontiers in Synaptic Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-08-29
- Volume
- 10
- Pages
- 29-29
- ISSN
- 1663-3563 (ISSN-L)
- PMC
- PMC6123351
- OpenAlex
- W2889177916
- Cited by
- 209
- References
- 23
- Citations by year
- 2026: 11 · 2025: 22 · 2024: 20 · 2023: 30 · 2022: 26 · 2021: 41 · 2020: 40 · 2019: 17 · 2014: 1 · 2012: 1
- FWCI
- 3.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Synaptic Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Mental Health (R01MH080047, R01MH111486)
- National Institute of Neurological Disorders and Stroke (DP1NS096787)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- dendritic spines, synaptic plasticity, local signaling, cytoskeletal remodeling, postsynaptic compartment, protein synthesis, calcium signaling, spatiotemporal signaling, learning and memory
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