ArticleThe Journal of cell biology2014
Munc18-1 redistributes in nerve terminals in an activity- and PKC-dependent manner.
Article in The Journal of cell biology, 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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Who cites it
31 citing papers in PubMed.
- Non-Synaptic Function and Localization of Syntaxin-Binding Protein 1 in a Mouse Model of STXBP1-Related Epileptic Encephalopathy.Annals of neurology · 2026Article
- Dynamic structural plasticity facilitates the developmental assembly of cochlear inner hair cell ribbon synapses.Frontiers in cell and developmental biology · 2026Article
- Article
- Convergence of autism proteins at the cilium.bioRxiv : the preprint server for biology · 2025Article
- Integrative analysis of long noncoding RNAs dysregulation and synapse-associated ceRNA regulatory axes in autism.Translational psychiatry · 2023Article
- Maximal Fusion Capacity and Efficient Replenishment of the Dense Core Vesicle Pool in Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- Article
- RNA editing-mediated regulation of calcium-dependent activator protein for secretion (CAPS1) localization and its impact on synaptic transmission.Journal of neurochemistry · 2021Article
- PTP-MEG2 regulates quantal size and fusion pore opening through two distinct structural bases and substrates.EMBO reports · 2021Article
- STXBP1 encephalopathies: Clinical spectrum, disease mechanisms, and therapeutic strategies.Journal of neurochemistry · 2021Review
- Role of Munc18-1 in the biological functions and pathogenesis of neurological disorders (Review).Molecular medicine reports · 2021Review
- Homozygous STXBP1 variant causes encephalopathy and gain-of-function in synaptic transmission.Brain : a journal of neurology · 2020Article
- BDNF-TrkB Signaling Coupled to nPKCε and cPKCβI Modulate the Phosphorylation of the Exocytotic Protein Munc18-1 During Synaptic Activity at the Neuromuscular Junction.Frontiers in molecular neuroscience · 2018Article
- MUNC18-1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development.Acta neuropathologica communications · 2017Article
- Diverse modes of synaptic signaling, regulation, and plasticity distinguish two classes ofeLife · 2017Article
- A Calcium- and Diacylglycerol-Stimulated Protein Kinase C (PKC), Caenorhabditis elegans PKC-2, Links Thermal Signals to Learned Behavior by Acting in Sensory Neurons and Intestinal Cells.Molecular and cellular biology · 2017Article
- Levetiracetam Affects Differentially Presynaptic Proteins in Rat Cerebral Cortex.Frontiers in cellular neuroscience · 2017Article
- Bassoon and piccolo regulate ubiquitination and link presynaptic molecular dynamics with activity-regulated gene expression.The Journal of physiology · 2016Review
- Presynaptic inhibition upon CB1 or mGlu2/3 receptor activation requires ERK/MAPK phosphorylation of Munc18-1.The EMBO journal · 2016Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Munc18-1 is a soluble protein essential for synaptic transmission. To investigate the dynamics of endogenous Munc18-1 in neurons, we created a mouse model expressing fluorescently tagged Munc18-1 from the endogenous munc18-1 locus. We show using fluorescence recovery after photobleaching in hippocampal neurons that the majority of Munc18-1 trafficked through axons and targeted to synapses via lateral diffusion together with syntaxin-1. Munc18-1 was strongly expressed at presynaptic terminals, with individual synapses showing a large variation in expression. Axon-synapse exchange rates of Munc18-1 were high: during stimulation, Munc18-1 rapidly dispersed from synapses and reclustered within minutes. Munc18-1 reclustering was independent of syntaxin-1, but required calcium influx and protein kinase C (PKC) activity. Importantly, a PKC-insensitive Munc18-1 mutant did not recluster. We show that synaptic Munc18-1 levels correlate with synaptic strength, and that synapses that recruit more Munc18-1 after stimulation have a larger releasable vesicle pool. Hence, PKC-dependent dynamic control of Munc18-1 levels enables individual synapses to tune their output during periods of activity.
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