Biochemical Computation for Spine Structural Plasticity
Open accessAbstract
The structural plasticity of dendritic spines is considered to be essential for various forms of synaptic plasticity, learning, and memory. The process is mediated by a complex signaling network consisting of numerous species of molecules. Furthermore, the spatiotemporal dynamics of the biochemical signaling are regulated in a complicated manner because of geometrical restrictions from the unique morphology of the dendritic branches and spines. Recent advances in optical techniques have enabled the exploration of the spatiotemporal aspects of the signal regulations in spines and dendrites and have provided many insights into the principle of the biochemical computation that underlies spine structural plasticity.
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There is compelling evidence that CaMKII, via phosphorylation, initiates a series of actin-based cytoskeletal rearrangements in the spine.
“Indeed, there is compelling evidence that CaMKII, via phosphorylation, initiates a series of actin-based cytoskeletal rearrangements in the spine (32, 312–314).”
From Synaptic memory and CaMKII (2023) · cites this paper as [313]
The ‘Calcium sensing’ and ‘Regulation of actin cytoskeleton’ sections describe CaMKII as an early spine-specific signal in LTP and place actin-remodeling pathways downstream of it. They do not establish the claim’s specific mechanism that CaMKII initiates those rearrangements via phosphorylation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe 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 [313]
The Rho GTPases Cdc42 and RhoA are required for LTP and sLTP.
“and that the Rho GTPases Cdc42 and RhoA are required for LTP and sLTP (312, 313).”
From Synaptic memory and CaMKII (2023) · cites this paper as [313]
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- Authors
- Nishiyama, J., & Yasuda, R.
- Affiliations
- Max Planck Florida Institute for Neuroscience (US)
- Corresponding author
- Yasuda, Ryohei
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 87
- Issue
- 1
- Pages
- 63-75
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4722820
- OpenAlex
- W1597375909
- Cited by
- 199
- References
- 154
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 15 · 2023: 10 · 2022: 21 · 2021: 21 · 2020: 23 · 2019: 20 · 2018: 25 · 2017: 23 · 2016: 19 · 2015: 2
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- National Institute of Mental Health (R01MH064748, R01MH080047, R01MH095090)
- National Institute of Neurological Disorders and Stroke (R01NS068410)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- dendritic spines, synaptic plasticity, biochemical signaling, spatiotemporal control, dendritic morphology, learning and memory, signaling networks
- MeSH terms
- Dendrites, Humans, Learning, Neuronal Plasticity, Signal Transduction, Long-Term Potentiation, Dendritic Spines
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