ArticleNature2016
The calcium sensor synaptotagmin 7 is required for synaptic facilitation.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
188 citing papers in PubMed, 1 synthesis or guideline pooled it, 367 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
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- Alternative splicing of synaptotagmin 7 regulates oligomerization and short-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A computational theory of short-term synaptic plasticity: synapses learn to tell time.Research square · 2026Article
- Presynaptic CabioRxiv : the preprint server for biology · 2026Article
- A Fast Synaptic Parameter Estimation Method Based on First- and Second-Order Moments for Short-Term Facilitating Synapses.Biomedicines · 2026Article
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- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Functional Nano-segregation of Distinct Forms of Neurotransmission.Advances in neurobiology · 2026Review
- Increase in Ia Afferent Synaptic Excitation of SOD1 G93A Mouse Motoneurons by 2-Week Anodal Trans-Spinal Direct Current Stimulation Does Not Ameliorate the Cellular Burden of the Disease.The European journal of neuroscience · 2025Article
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- Independently engaging protein tethers of different length enhance synaptic vesicle trafficking to the plasma membrane.The Journal of physiology · 2025Article
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025Review
- Intersectin and endophilin condensates prime synaptic vesicles for release site replenishment.Nature neuroscience · 2025Article
- Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.Biophysical journal · 2025Article
- Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Synaptotagmin-7 deficit causes insulin hypoactivity and contributes to behavioral alterations in mice.iScience · 2025Article
- SYT7 accelerates nasopharyngeal carcinoma progression via ALDH1A3-mediated STAT3 signaling activation.Oncogenesis · 2025Article
128 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
It has been known for more than 70 years that synaptic strength is dynamically regulated in a use-dependent manner. At synapses with a low initial release probability, closely spaced presynaptic action potentials can result in facilitation, a short-term form of enhancement in which each subsequent action potential evokes greater neurotransmitter release. Facilitation can enhance neurotransmitter release considerably and can profoundly influence information transfer across synapses, but the underlying mechanism remains a mystery. One proposed mechanism is that a specialized calcium sensor for facilitation transiently increases the probability of release, and this sensor is distinct from the fast sensors that mediate rapid neurotransmitter release. Yet such a sensor has never been identified, and its very existence has been disputed. Here we show that synaptotagmin 7 (Syt7) is a calcium sensor that is required for facilitation at several central synapses. In Syt7-knockout mice, facilitation is eliminated even though the initial probability of release and the presynaptic residual calcium signals are unaltered. Expression of wild-type Syt7 in presynaptic neurons restored facilitation, whereas expression of a mutated Syt7 with a calcium-insensitive C2A domain did not. By revealing the role of Syt7 in synaptic facilitation, these results resolve a longstanding debate about a widespread form of short-term plasticity, and will enable future studies that may lead to a deeper understanding of the functional importance of facilitation.
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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.