ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Munc13-3 superprimes synaptic vesicles at granule cell-to-basket cell synapses in the mouse cerebellum.
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 31 papers.
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31 citing papers in PubMed, 41 citations in OpenAlex.
- Astroglial modulation of synaptic function in the non-demyelinated cerebellar cortex is dependent on MyD88 signaling in a model of toxic demyelination.Journal of neuroinflammation · 2025Article
- Role of the UNC13 family in human diseases: A literature review.AIMS neuroscience · 2023Review
- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- Functional Roles of UNC-13/Munc13 and UNC-18/Munc18 in Neurotransmission.Advances in neurobiology · 2023Review
- A fluorescent nanosensor paint detects dopamine release at axonal varicosities with high spatiotemporal resolution.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A two-subpopulation model that reflects heterogeneity of large dense core vesicles in exocytosis.Cell cycle (Georgetown, Tex.) · 2022Article
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- Regulation of a subset of release-ready vesicles by the presynaptic protein Mover.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- β-Adrenergic Receptors/Epac Signaling Increases the Size of the Readily Releasable Pool of Synaptic Vesicles Required for Parallel Fiber LTP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Heterogeneous Presynaptic Distribution of Munc13 Isoforms at Retinal Synapses and Identification of an Unconventional Bipolar Cell Type with Dual Expression of Munc13 Isoforms: A Study Using Munc13-EXFP Knock-in Mice.International journal of molecular sciences · 2020Article
- Incomplete vesicular docking limits synaptic strength under high release probability conditions.eLife · 2020Article
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- What We Can Learn From Cumulative Numbers of Vesicular Release Events.Frontiers in cellular neuroscience · 2019Article
- Control of Presynaptic Parallel Fiber Efficacy by Activity-Dependent Regulation of the Number of Occupied Release Sites.Frontiers in systems neuroscience · 2019Article
- Apparent calcium dependence of vesicle recruitment.The Journal of physiology · 2018Article
- A two-step docking site model predicting different short-term synaptic plasticity patterns.The Journal of general physiology · 2018Article
- Doc2-mediated superpriming supports synaptic augmentation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Synaptotagmin CaFrontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Munc13-3 is a presynaptic protein implicated in vesicle priming that is strongly expressed in cerebellar granule cells (GCs). Mice deficient of Munc13-3 (Munc13-3(-/-)) show an increased paired-pulse ratio (PPR), which led to the hypothesis that Munc13-3 increases the release probability (pr) of vesicles. In the present study, we analyzed unitary synaptic connections between GCs and basket cells in acute cerebellar slices from wild-type and Munc13-3(-/-) mice. Unitary EPSCs recorded from Munc13-3(-/-) GCs showed normal kinetics and synaptic latency but a significantly increased PPR and fraction of synaptic failures. A quantal analysis revealed that neither the charge of single quanta nor the binominal parameter N were affected by loss of Munc13-3 but that pr was almost halved in Munc13-3(-/-). Neither presynaptic Ca(2+) influx was affected by deletion of Munc13-3 nor replenishment of the readily releasable vesicle pool. However, a high concentration of EGTA led to a reduction in EPSCs that was significantly stronger in Munc13-3(-/-). We conclude that Munc13-3 is responsible for an additional step of molecular and/or positional "superpriming" that substantially increases the efficacy of Ca(2+)-triggered release.
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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.