ArticleNature neuroscience2025
Intersectin and endophilin condensates prime synaptic vesicles for release site replenishment.
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- CAST/ELKS-endophilin-A interaction ensures synaptic vesicle pool size.The Journal of cell biology · 2026Article
- Physiological implications of phase separation in vesicle organization and trafficking.BMC biology · 2026Review
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Single-vesicle imaging reveals actin-dependent spatial restriction of vesicles at the active zone, essential for sustained transmission.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The juxtamembrane linker of synaptotagmin 1 regulates CaNature communications · 2024Article
- Dipping contacts - a novel type of contact site at the interface between membraneless organelles and membranes.Journal of cell science · 2023Article
- The juxtamembrane linker of synaptotagmin 1 regulates CabioRxiv : the preprint server for biology · 2023Article
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Authors and funding
14 authors.
Funding
Abstract
Following synaptic vesicle fusion, vacated release sites are replenished immediately by new vesicles for subsequent neurotransmission. These replacement vesicles are assumed to be located near release sites and used by chance. Here we find in mouse hippocampal excitatory synapses that replacement vesicles are clustered near the active zone where release sites reside by intersectin-1. Specifically, intersectin-1 forms dynamic molecular condensates with endophilin A1 and sequesters vesicles around this region. In the absence of intersectin-1, fewer vesicles cluster within 20 nm of the plasma membrane, and consequently vacated sites cannot be replenished rapidly, leading to synaptic depression. Mutations in intersectin-1 that disrupt endophilin A1 binding result in similar phenotypes. In the absence of endophilin A1, intersectin-1 is mislocalized, and this replacement pool of vesicles cannot be accessed, suggesting that endophilin A1 is needed to mobilize these vesicles. Thus, our work describes the replacement zone within a synapse, where replacement vesicles are stored for replenishment of the release site.
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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 Socratic graph.