Synaptic Vesicle Endocytosis

Saheki, Y.; De Camilli, P.

doi:10.1101/cshperspect.a005645

Cited by 457Cellular transport and secretionNeuroscience and Neuropharmacology ResearchExtracellular vesicles in disease

Synaptic Vesicle Endocytosis

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Saheki, Y., De Camilli, P.·2012·Cold Spring Harbor Perspectives in Biology

DOI 10.1101/cshperspect.a005645PMC PMC3428771

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Abstract

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.
“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]
The paper’s introductory discussion describes clathrin-mediated and bulk endocytosis and presents kiss-and-run as a possible third pathway. The KISS AND RUN section says its evidence remains primarily indirect, and our copy does not identify ultrafast endocytosis as a separate pathway (searched: “ultrafast” and “ultra-fast”). (LLM, conf=0.88)
Experimental — accuracy not yet measured
Bulk endocytosis is triggered by intense or prolonged neuronal stimulation and involves retrieval of large portions of the plasma membrane as large endocytic vacuoles, from which new SVs are regenerated through clathrin-mediated budding.
“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]
The BULK ENDOCYTOSIS section says this pathway is prominent under strong stimulation and recaptures plasma membrane into vacuoles and cisternae. It also says that how those vacuoles become new synaptic vesicles remains unresolved; it presents clathrin-dependent budding as a possibility, not an established mechanism. In the printed citing sentence, the clathrin-mediated budding statement carries separate citations [12,31]. (LLM, conf=0.90)
Experimental — accuracy not yet measured
Clathrin-mediated endocytosis (CME) is the most prevalent pathway for SV retrieval, involving clathrin-coated pits that bud off within tens of seconds following full-collapse fusion.
“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]
The Clathrin-Mediated Endocytosis section describes abundant clathrin-dependent synaptic-vesicle recycling, and Clathrin Coats and the Genesis of a Synaptic Vesicle describes coated pits budding from the membrane. The copy does not establish that CME is the most prevalent pathway or that coated pits internalize vesicle components within tens of seconds specifically after full-collapse fusion. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Exocytosis is responsible for release of neurotransmitters, while endocytosis is responsible for recycling of synaptic vesicle membranes.
“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]
At the synapse, release of neurotransmitters relies on exocytosis and endocytosis.
“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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Botulinum Neurotoxins: Biology, Pharmacology, and Toxicology
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Self-citation
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Synaptic Vesicle Endocytosis Occurs on Multiple Timescales and Is Mediated by Formin-Dependent Actin Assembly
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Synaptic Vesicle Endocytosis in Different Model Systems
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A Recurrent Missense Variant in AP2M1 Impairs Clathrin-Mediated Endocytosis and Causes Developmental and Epileptic Encephalopathy
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Actin Is Crucial for All Kinetically Distinguishable Forms of Endocytosis at Synapses
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Dynamin is primed at endocytic sites for ultrafast endocytosis
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Insights into VPS13 properties and function reveal a new mechanism of eukaryotic lipid transport
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Presynaptic autophagy is coupled to the synaptic vesicle cycle via ATG-9
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α-Synuclein: A Multifunctional Player in Exocytosis, Endocytosis, and Vesicle Recycling
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Exosome: A novel neurotransmission modulator or non-canonical neurotransmitter?
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Research progress on the role of type I vesicular glutamate transporter (VGLUT1) in nervous system diseases
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Loss of SYNJ1 dual phosphatase activity leads to early onset refractory seizures and progressive neurological decline
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An overview of the synaptic vesicle lipid composition
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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)
DOI: 10.1101/cshperspect.a005645
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

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