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Developmental regulation of spine motility in the mammalian central nervous system
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The function of dendritic spines, postsynaptic sites of excitatory input in the mammalian central nervous system (CNS), is still not well understood. Although changes in spine morphology may mediate synaptic plasticity, the extent of basal spine motility and its regulation and function remains controversial. We investigated spine motility in three principal neurons of the mouse CNS: cerebellar Purkinje cells, and cortical and hippocampal pyramidal neurons. Motility was assayed with time-lapse imaging by using two-photon microscopy of green fluorescent protein-labeled neurons in acute and cultured slices. In all three cell types, dendritic protrusions (filopodia and spines) were highly dynamic, exhibiting a diversity of morphological rearrangements over short (<1-min) time courses. The incidence of spine motility declined during postnatal maturation, but dynamic changes were still apparent in many spines in late-postnatal neurons. Although blockade or induction of neuronal activity did not affect spine motility, disruption of actin polymerization did. We hypothesize that this basal motility of dendritic protrusions is intrinsic to the neuron and underlies the heightened plasticity found in developing CNS.
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“Because spine motility rates decrease during development (Dunaevsky et al., 1999; Majewska and Sur, 2003), this measure is a mark of synapse maturation.”
From Pathogenic SYNGAP1 Mutations Impair Cognitive Development by Disrupting Maturation of Dendritic Spine Synapses (2012) · cites this paper as Dunaevsky et al., 1999
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Metadata
- Authors
- Dunaevsky, A., Tashiro, A., Majewska, A., Mason, C., & Yuste, R.
- Affiliations
- Columbia University (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1999-11-09
- Volume
- 96
- Issue
- 23
- Pages
- 13438-13443
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC23966
- OpenAlex
- W2156678388
- Cited by
- 412
- References
- 39
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 9 · 2022: 10 · 2021: 9 · 2020: 12 · 2019: 8 · 2018: 8 · 2017: 9 · 2016: 9 · 2015: 11 · 2014: 21 · 2013: 12 · 2012: 16
- FWCI
- 7.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Columbia Academic Commons (Columbia University)
- Funders
- National Institutes of Health
- National Eye Institute (R01 EY111787)
- National Institute of Neurological Disorders and Stroke (F32NS010370, R01 NS16951, NS10370, R01NS016951)
- National Institute of Environmental Health Sciences (R01ES016951)
- 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 › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- dendritic protrusions, filopodia, postnatal development, synaptic plasticity, Purkinje cells, pyramidal neurons, hippocampal neurons, actin polymerization, neuronal activity, dendritic morphology, central nervous system development
- MeSH terms
- Animals, Brain, Dendrites, Luminescent Proteins, Mice, Inbred C57BL, Green Fluorescent Proteins, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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