ArticleScientific reports2016
State-dependent diffusion of actin-depolymerizing factor/cofilin underlies the enlargement and shrinkage of dendritic spines.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- N-Homocysteinylation of Cofilin-1 Aggravates Epileptic Pathophysiology via Disruption of Actin Dynamics.Neuroscience bulletin · 2026Article
- NMDA receptor-dependent structural plasticity links early life stress to persistent aggression.Neurobiology of stress · 2026Review
- Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026Review
- Long-term potentiation-induced changes in actin dynamics and spine geometry persist on the timescale of the synaptic tag.Communications biology · 2025Article
- Synaptic Plasticity Linked to Ionotropic Glutamate Receptors After Nicotine Exposure.Current neuropharmacology · 2025Review
- Structural and functional alterations of neurons derived from sporadic Alzheimer's disease hiPSCs are associated with downregulation of the LIMK1-cofilin axis.Alzheimer's research & therapy · 2024Article
- STING Driving Synaptic Phagocytosis of Hippocampal Microglia/Macrophages Contributes to Cognitive Impairment in Sepsis-Associated Encephalopathy in Mice.CNS neuroscience & therapeutics · 2024Article
- PI3K couples long-term synaptic potentiation with cofilin recruitment and actin polymerization in dendritic spines via its regulatory subunit p85α.Cellular and molecular life sciences : CMLS · 2024Article
- H-Ras induces exuberantiScience · 2024Article
- Altered projection-specific synaptic remodeling and its modification by oxytocin in an idiopathic autism marmoset model.Communications biology · 2024Article
- Local and global predictors of synapse elimination during motor learning.Science advances · 2024Article
- Engineering memory with an extrinsically disordered kinase.Science advances · 2023Article
- Article
- Unraveling the mysteries of dendritic spine dynamics: Five key principles shaping memory and cognition.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023Article
- Regulation of dendritic spines in the amygdala following sleep deprivation.Frontiers in sleep · 2023Article
- Dendritic autophagy degrades postsynaptic proteins and is required for long-term synaptic depression in mice.Nature communications · 2022Article
- Stress-induced vulnerability to develop cocaine addiction depends on cofilin modulation.Neurobiology of stress · 2021Article
- Enhancing motor learning by increasing the stability of newly formed dendritic spines in the motor cortex.Neuron · 2021Article
- Review
- Spine dynamics in the brain, mental disorders and artificial neural networks.Nature reviews. Neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic spines are the postsynaptic sites of most excitatory synapses in the brain, and spine enlargement and shrinkage give rise to long-term potentiation and depression of synapses, respectively. Because spine structural plasticity is accompanied by remodeling of actin scaffolds, we hypothesized that the filamentous actin regulatory protein cofilin plays a crucial role in this process. Here we investigated the diffusional properties of cofilin, the actin-severing and depolymerizing actions of which are activated by dephosphorylation. Cofilin diffusion was measured using fluorescently labeled cofilin fusion proteins and two-photon imaging. We show that cofilins are highly diffusible along dendrites in the resting state. However, during spine enlargement, wild-type cofilin and a phosphomimetic cofilin mutant remain confined to the stimulated spine, whereas a nonphosphorylatable mutant does not. Moreover, inhibition of cofilin phosphorylation with a competitive peptide disables spine enlargement, suggesting that phosphorylated-cofilin accumulation is a key regulator of enlargement, which is localized to individual spines. Conversely, spine shrinkage spreads to neighboring spines, even though triggered by weaker stimuli than enlargement. Diffusion of exogenous cofilin injected into a pyramidal neuron soma causes spine shrinkage and reduced PSD95 in spines, suggesting that diffusion of dephosphorylated endogenous cofilin underlies the spreading of spine shrinkage and long-term depression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.