ArticleProceedings of the National Academy of Sciences of the United States of America2024
Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed.
- A primordial synaptotagmin-independent function of complexin in regulated exocytosis.Nature communications · 2026Article
- Postsynaptic Complexin Mediates Constitutive Exocytosis of Nicotinic Acetylcholine Receptor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Calorie Restriction Effects on Aging, Learning Performance, and Transcription in Aged Aplysia californica.Genes, brain, and behavior · 2026Article
- Role of complexin 2 in the regulation of hormone secretion from the islet of Langerhans.American journal of physiology. Endocrinology and metabolism · 2025Article
- Complexin gains effective access to the assembling SNAREs via its membrane-binding C-terminal domain.The Journal of physiology · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- A Conceptual Review of Naturally Occurring Toxins and Venoms as Peptide Blockers to Combat Chronic Low Back Pain.JOR spine · 2025Review
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- Exploring the structural dynamics of the vesicle priming machinery.Biochemical Society transactions · 2024Review
- Synaptotagmins 3 and 7 mediate the majority of asynchronous release from synapses in the cerebellum and hippocampus.Cell reports · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The presynaptic SNARE-complex regulator complexin (Cplx) enhances the fusogenicity of primed synaptic vesicles (SVs). Consequently, Cplx deletion impairs action potential-evoked transmitter release. Conversely, though, Cplx loss enhances spontaneous and delayed asynchronous release at certain synapse types. Using electrophysiology and kinetic modeling, we show that such seemingly contradictory transmitter release phenotypes seen upon Cplx deletion can be explained by an additional of Cplx in the control of SV priming, where its ablation facilitates the generation of a "faulty" SV fusion apparatus. Supporting this notion, a sequential two-step priming scheme, featuring reduced vesicle fusogenicity and increased transition rates into the faulty primed state, reproduces all aberrations of transmitter release modes and short-term synaptic plasticity seen upon Cplx loss. Accordingly, we propose a dual presynaptic function for the SNARE-complex interactor Cplx, one as a "checkpoint" protein that guarantees the proper assembly of the fusion machinery during vesicle priming, and one in boosting vesicle fusogenicity.
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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 Socratic graph.