ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Presynaptic clathrin levels are a limiting factor for synaptic transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- ERICH3: vesicular association and antidepressant treatment response.Molecular psychiatry · 2021Pooled it
- Synaptic Vesicle Recycling at the Developing Presynapse.Journal of neurochemistry · 2025Review
- Altered tear fluid protein expression in persons with mild Alzheimer's disease in proteins involved in oxidative stress, protein synthesis, and energy metabolism.Journal of Alzheimer's disease : JAD · 2025Article
- Microtubule depolymerization contributes to spontaneous neurotransmitter release in vitro.Communications biology · 2023Article
- FMRP Sustains Presynaptic Function via Control of Activity-Dependent Bulk Endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Synapse elimination activates a coordinated homeostatic presynaptic response in an autaptic circuit.Communications biology · 2020Article
- Btbd3 expression regulates compulsive-like and exploratory behaviors in mice.Translational psychiatry · 2019Article
- An integrated transcriptomics and proteomics analysis reveals functional endocytic dysregulation caused by mutations in LRRK2.Neurobiology of disease · 2019Article
- Recycling at synapses.eLife · 2016Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
- Article
- SPARC triggers a cell-autonomous program of synapse elimination.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Synaptic vesicle exocytosis and increased cytosolic calcium are both necessary but not sufficient for activity-dependent bulk endocytosis.Journal of neurochemistry · 2015Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
To maintain communication, neurons must recycle their synaptic vesicles with high efficiency. This process places a huge burden on the clathrin-mediated endocytic machinery, but the consequences of this are poorly understood. We found that the amount of clathrin in a presynaptic terminal is not fixed. During stimulation, clathrin moves out of synapses as a function of stimulus strength and neurotransmitter release probability, which, together with membrane coat formation, transiently reduces the available pool of free clathrin triskelia. Correlative functional and morphological experiments in cholinergic autapses established by superior cervical ganglion neurons in culture show that presynaptic terminal function is compromised if clathrin levels fall by 20% after clathrin heavy chain knock down using RNAi. Synaptic transmission is depressed due to a reduction of cytoplasmic and readily releasable pools of vesicles. However, synaptic depression reverts after dialysis of exogenous clathrin, thus compensating RNAi-induced depletion. Lowering clathrin levels also reduces quantal size, which occurs concomitantly with a decrease in the size of synaptic vesicles. Large dense-core vesicles are unaffected by clathrin knock down. Together, our results show that clathrin levels are a dynamic property of presynaptic terminals that can influence short-term plasticity in a stimulus-dependent manner.
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Registered trials
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