ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Synapsin selectively controls the mobility of resting pool vesicles at hippocampal terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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Who cites it
50 citing papers in PubMed, 85 citations in OpenAlex.
- Dynamic regulation of vesicle pools in a detailed spatial model of the complete synaptic vesicle cycle.Science advances · 2025Article
- Synaptic vesicle-omics in mice captures signatures of aging and synucleinopathy.Nature communications · 2025Article
- Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
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- Synapsin condensation controls synaptic vesicle sequestering and dynamics.Nature communications · 2023Article
- Adaptor protein AP-3 produces synaptic vesicles that release at high frequency by recruiting phospholipid flippase ATP8A1.Nature neuroscience · 2023Article
- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
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- Functional and Pathological Effects of α-Synuclein on Synaptic SNARE Complexes.Journal of molecular biology · 2023Review
- Invertebrate neurons as a simple model to study the hyperexcitable state of epileptic disorders in single cells, monosynaptic connections, and polysynaptic circuits.Biophysical reviews · 2022Review
- CDH2 mutation affecting N-cadherin function causes attention-deficit hyperactivity disorder in humans and mice.Nature communications · 2021Article
- The endosomal Q-SNARE, Syntaxin 7, defines a rapidly replenishing synaptic vesicle recycling pool in hippocampal neurons.Communications biology · 2021Article
- Axon terminals control endolysosome diffusion to support synaptic remodelling.Life science alliance · 2021Article
- Synuclein Regulates Synaptic Vesicle Clustering and Docking at a Vertebrate Synapse.Frontiers in cell and developmental biology · 2021Article
- α-Synuclein facilitates endocytosis by elevating the steady-state levels of phosphatidylinositol 4,5-bisphosphate.The Journal of biological chemistry · 2020Article
- Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO.Nature communications · 2020Article
- Article
- Sparse force-bearing bridges between neighboring synaptic vesicles.Brain structure & function · 2019Article
- Article
- Synapsins regulate α-synuclein functions.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Presynaptic terminals are specialized sites for information transmission where vesicles fuse with the plasma membrane and are locally recycled. Recent work has extended this classical view, with the observation that a subset of functional vesicles is dynamically shared between adjacent terminals by lateral axonal transport. Conceptually, such transport would be expected to disrupt vesicle retention around the active zone, yet terminals are characterized by a high-density vesicle cluster, suggesting that counteracting stabilizing mechanisms must operate against this tendency. The synapsins are a family of proteins that associate with synaptic vesicles and determine vesicle numbers at the terminal, but their specific function remains controversial. Here, using multiple quantitative fluorescence-based approaches and electron microscopy, we show that synapsin is instrumental for resisting vesicle dispersion and serves as a regulatory element for controlling lateral vesicle sharing between synapses. Deleting synapsin disrupts the organization of presynaptic vesicle clusters, making their boundaries hard to define. Concurrently, the fraction of vesicles amenable to transport is increased, and more vesicles are translocated to the axon. Importantly, in neurons from synapsin knock-out mice the resting and recycling pools are equally mobile. Synapsin, when present, specifically restricts the mobility of resting pool vesicles without affecting the division of vesicles between these pools. Specific expression of synapsin IIa, the sole isoform affecting synaptic depression, rescues the knock-out phenotype. Together, our results show that synapsin is pivotal for maintaining synaptic vesicle cluster integrity and that it contributes to the regulated sharing of vesicles between terminals.
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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.