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Synaptic Vesicle Endocytosis
Open accessAbstract
Neurons can sustain high rates of synaptic transmission without exhausting their supply of synaptic vesicles. This property relies on a highly efficient local endocytic recycling of synaptic vesicle membranes, which can be reused for hundreds, possibly thousands, of exo-endocytic cycles. Morphological, physiological, molecular, and genetic studies over the last four decades have provided insight into the membrane traffic reactions that govern this recycling and its regulation. These studies have shown that synaptic vesicle endocytosis capitalizes on fundamental and general endocytic mechanisms but also involves neuron-specific adaptations of such mechanisms. Thus, investigations of these processes have advanced not only the field of synaptic transmission but also, more generally, the field of endocytosis. This article summarizes current information on synaptic vesicle endocytosis with an emphasis on the underlying molecular mechanisms and with a special focus on clathrin-mediated endocytosis, the predominant pathway of synaptic vesicle protein internalization.
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“Following exocytosis, synaptic vesicles are recovered through clathrin-mediated, ultrafast, bulk, or kiss-and-run endocytic pathways.”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [30]
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“Bulk endocytosis is triggered by intense or prolonged neuronal stimulation. This pathway involves the retrieval of large portions of the plasma membrane in the form of large endocytic vacuoles [30]. New SVs are subsequently regenerated from these larger structures through clathrin-mediated budding [12,31].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [30]
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“Clathrin-mediated endocytosis (CME) is the most prevalent pathway for SV retrieval. It involves the formation of clathrin-coated pits that bud off from the plasma membrane, internalizing SV components within tens of seconds following full-collapse fusion [30,31].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [30]
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“The process of exocytosis is responsible for the release of neurotransmitters, while the process of endocytosis is responsible for the recycling of the synaptic vesicle membranes [148].”
From Insights of Endocytosis Signaling in Health and Disease (2023) · cites this paper as [148]
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“At the synapse, the release of neurotransmitters relies on the two fundamental biological events, such as exocytosis and endocytosis.”
From Insights of Endocytosis Signaling in Health and Disease (2023) · cites this paper as [148]
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“After exocytosis, vesicle membrane must be retrieved from the plasma membrane through endocytosis to keep the area of the plasma membrane constant and maintain a sufficient number of synaptic vesicles at presynapses1–4.”
From Membrane compression by synaptic vesicle exocytosis triggers ultrafast endocytosis (2023) · cites this paper as [2]
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“After exocytosis, vesicle membrane must be retrieved from the plasma membrane through endocytosis to keep the area of the plasma membrane constant and maintain a sufficient number of synaptic vesicles at presynapses1–4.”
From Membrane compression by synaptic vesicle exocytosis triggers ultrafast endocytosis (2023) · cites this paper as [2]
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“Kiss-and-run is a rapid mechanism that involves a transient opening of a fusion pore, allowing for neurotransmitter release without full collapse of the SV into the plasma membrane [30]. The vesicle is then rapidly retrieved, often within approximately one second [31,32].”
From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [30]
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Chen, H., Slepnev, V. I., Di Fiore, P. P., & De Camilli, P. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.6.3257 · Cited by 138 · cited 2×
“…to as dephosphins , include proteins with different functions in endocytosis including dynamin, synaptojanin , PIPKIg, AP180, epsin, Eps15, and several others (Liu et al. 1994; McPherson et al. 1994; Chen et al. 1999; Cousin and Robinson 2001; Lee et al. 2004, 2005; Nakano-Kobayashi et al. 2007).”
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7 of the 297 references couldn’t be matched to a known paper.
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Botulinum Neurotoxins: Biology, Pharmacology, and Toxicology
Pirazzini, M., Rossetto, O., Eleopra, R., & Montecucco, C. (2017) · Pharmacological Reviews · doi:10.1124/pr.116.012658 · Cited by 776
Botulinum neurotoxins: genetic, structural and mechanistic insights
Rossetto, O., Pirazzini, M., & Montecucco, C. (2014) · Nature Reviews Microbiology · doi:10.1038/nrmicro3295 · Cited by 637
Virus Infections in the Nervous System
Koyuncu, O. O., Hogue, I. B., & Enquist, L. W. (2013) · Cell Host & Microbe · doi:10.1016/j.chom.2013.03.010 · Cited by 594
Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers
Sardar Sinha, M., Ansell-Schultz, A., Civitelli, L., Hildesjö, C., Larsson, M., Lannfelt, L., Ingelsson, M., & Hallbeck, M. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1868-1 · Cited by 527
Tau association with synaptic vesicles causes presynaptic dysfunction
Zhou, L., McInnes, J., Wierda, K., Holt, M., Herrmann, A. G., Jackson, R. J., Wang, Y.-C., Swerts, J., Beyens, J., Miskiewicz, K., et al. (2017) · Nature Communications · doi:10.1038/ncomms15295 · Cited by 434
Metadata
- Authors
- Saheki, Y., & De Camilli, P.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Saheki, Y.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-07-03
- Volume
- 4
- Issue
- 9
- Pages
- a005645-a005645
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC3428771
- OpenAlex
- W2804806451
- Cited by
- 457
- References
- 297
- Citations by year
- 2026: 32 · 2025: 20 · 2024: 24 · 2023: 32 · 2022: 38 · 2021: 32 · 2020: 40 · 2019: 38 · 2018: 30 · 2017: 41 · 2016: 33 · 2015: 37 · 2014: 36 · 2013: 17 · 2012: 4
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of Neurological Disorders and Stroke (R37NS036251)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Keywords
- synaptic vesicle endocytosis, synaptic vesicle recycling, clathrin-mediated endocytosis, synaptic transmission, membrane traffic, exocytosis
- MeSH terms
- Clathrin, Endocytosis, Exocytosis, Intracellular Membranes, Membrane Fusion, Actin Cytoskeleton, Models, Biological, Synaptic Transmission, Phosphatidylinositols, Synaptic Vesicles, Protein Transport, Clathrin-Coated Vesicles
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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