ArticleNature neuroscience2009
Ca(2+) and calmodulin initiate all forms of endocytosis during depolarization at a nerve terminal.
Article in Nature neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 147 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
147 citing papers in PubMed, 237 citations in OpenAlex.
- NSF is required for diverse endocytic modes by promoting fusion and fission pore closure in secretory cells.iScience · 2026Article
- Membrane Merger Dynamics in Exocytosis and Endocytosis.Advances in experimental medicine and biology · 2026Review
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- A phosphoinositide switch from PI(4,5)PScience advances · 2025Article
- An iPSC-derived neuronal model reveals manganese's role in neuronal endocytosis, calcium flux and mitochondrial bioenergetics.iScience · 2025Article
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- Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.Cell & bioscience · 2025Article
- SARS-CoV-2 Inhibits Exo-Endocytosis and Enhances Short-Term Depression at a Central Synapse.Neuroscience bulletin · 2025Article
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.Nature communications · 2024Article
- Clathrin mediates membrane fission and budding by constricting membrane pores.Cell discovery · 2024Article
- Membrane transformations of fusion and budding.Nature communications · 2024Review
- The CHD family chromatin remodeling enzyme, Kismet, promotes both clathrin-mediated and activity-dependent bulk endocytosis.PloS one · 2024Article
- Synaptotagmin-11 Inhibits Synaptic Vesicle Endocytosis via Endophilin A1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Calcium Dyshomeostasis Drives Pathophysiology and Neuronal Demise in Age-Related Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- An approach for quantitative mapping of synaptic periactive zone architecture and organization.Molecular biology of the cell · 2023Article
- Two forms of asynchronous release with distinctive spatiotemporal dynamics in central synapses.eLife · 2023Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedDosage error in article text
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Although endocytosis maintains synaptic transmission, how endocytosis is initiated is unclear. We found that calcium influx initiated all forms of endocytosis at a single nerve terminal in rodents, including clathrin-dependent slow endocytosis, bulk endocytosis, rapid endocytosis and endocytosis overshoot (excess endocytosis), with each being evoked with a correspondingly higher calcium threshold. As calcium influx increased, endocytosis gradually switched from very slow endocytosis to slow endocytosis to bulk endocytosis to rapid endocytosis and to endocytosis overshoot. The calcium-induced endocytosis rate increase was a result of the speeding up of membrane invagination and fission. Pharmacological experiments suggested that the calcium sensor mediating these forms of endocytosis is calmodulin. In addition to its role in recycling vesicles, calcium/calmodulin-initiated endocytosis facilitated vesicle mobilization to the readily releasable pool, probably by clearing fused vesicle membrane at release sites. Our findings provide a unifying mechanism for the initiation of various forms of endocytosis that are critical in maintaining exocytosis.
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Registered trials
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.