ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Complexin stabilizes newly primed synaptic vesicles and prevents their premature fusion at the mouse calyx of held synapse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it.
- GWAS meta-analysis reveals key risk loci in essential tremor pathogenesis.Communications biology · 2024Pooled it
- Blood-based proteomic signature of amyloidosis: identification of novel regulators of amyloid load.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- QuadST identifies cell-cell interaction-changed genes in spatially resolved transcriptomics data.Genome research · 2025Article
- CaScience advances · 2025Article
- The exocytosis regulator complexin controls spontaneous synaptic vesicle release in a CAPS-dependent manner at C. elegans excitatory synapses.PLoS biology · 2025Article
- CPLX1 is a novel prognostic biomarker in CRC correlating with immunotherapy resistance and ferroptosis.Frontiers in immunology · 2025Article
- Dynamic formation of the protein-lipid prefusion complex.Biophysical journal · 2024Article
- Direct neuronal reprogramming of mouse astrocytes is associated with multiscale epigenome remodeling and requires Yy1.Nature neuroscience · 2024Article
- Dynamic Formation of the Protein-Lipid Pre-fusion Complex.bioRxiv : the preprint server for biology · 2024Article
- Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-cell multi-omics analysis of lineage development and spatial organization in the human fetal cerebellum.Cell discovery · 2024Article
- Light-dependent regulation of neurotransmitter release from rod photoreceptor ribbon synapses involves an interplay of Complexin 4 and Transducin with the SNARE complex.Frontiers in molecular neuroscience · 2024Article
- REST-dependent glioma progression occurs independently of the repression of the long non-coding RNA HAR1A.PloS one · 2024Article
- QuadST: A Powerful and Robust Approach for Identifying Cell-Cell Interaction-Changed Genes on Spatially Resolved Transcriptomics.bioRxiv : the preprint server for biology · 2023Article
- An Alzheimer's disease risk variant in TTC3 modifies the actin cytoskeleton organization and the PI3K-Akt signaling pathway in iPSC-derived forebrain neurons.Neurobiology of aging · 2023Article
- Group I metabotropic glutamate receptor-triggered temporally patterned action potential-dependent spontaneous synaptic transmission in mouse MNTB neurons.Hearing research · 2023Article
- Review
- Complexin Membrane Interactions: Implications for Synapse Evolution and Function.Journal of molecular biology · 2023Review
- Complexins: Ubiquitously Expressed Presynaptic Regulators of SNARE-Mediated Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complexins (Cplxs) are small synaptic proteins that cooperate with SNARE-complexes in the control of synaptic vesicle (SV) fusion. Studies involving genetic mutation, knock-down, or knock-out indicated two key functions of Cplx that are not mutually exclusive but cannot easily be reconciled, one in facilitating SV fusion, and one in "clamping" SVs to prevent premature fusion. Most studies on the role of Cplxs in mammalian synapse function have relied on cultured neurons, heterologous expression systems, or membrane fusion assays in vitro, whereas little is known about the function of Cplxs in native synapses. We therefore studied consequences of genetic ablation of Cplx1 in the mouse calyx of Held synapse, and discovered a developmentally exacerbating phenotype of reduced spontaneous and evoked transmission but excessive asynchronous release after stimulation, compatible with combined facilitating and clamping functions of Cplx1. Because action potential waveforms, Ca(2+) influx, readily releasable SV pool size, and quantal size were unaltered, the reduced synaptic strength in the absence of Cplx1 is most likely a consequence of a decreased release probability, which is caused, in part, by less tight coupling between Ca(2+) channels and docked SV. We found further that the excessive asynchronous release in Cplx1-deficient calyces triggered aberrant action potentials in their target neurons, and slowed-down the recovery of EPSCs after depleting stimuli. The augmented asynchronous release had a delayed onset and lasted hundreds of milliseconds, indicating that it predominantly represents fusion of newly recruited SVs, which remain unstable and prone to premature fusion in the absence of Cplx1.
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