ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Activity-dependent fusion pore expansion regulated by a calcineurin-dependent dynamin-syndapin pathway in mouse adrenal chromaffin cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Deployment of endocytic machinery to periactive zones of nerve terminals is independent of active zone assembly and evoked release.bioRxiv : the preprint server for biology · 2026Article
- Omega-3 and -6 Fatty Acids Alter the Membrane Lipid Composition and Vesicle Size to Regulate Exocytosis and Storage of Catecholamines.ACS chemical neuroscience · 2024Article
- PACSIN proteins in vivo: Roles in development and physiology.Acta physiologica (Oxford, England) · 2022Review
- Regulating quantal size of neurotransmitter release through a GPCR voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Spatiotemporal organization and protein dynamics involved in regulated exocytosis of MMP-9 in breast cancer cells.The Journal of general physiology · 2019Article
- Plasticity in exocytosis revealed through the effects of repetitive stimuli affect the content of nanometer vesicles and the fraction of transmitter released.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Dynamin 1 Restrains Vesicular Release to a Subquantal Mode In Mammalian Adrenal Chromaffin Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Local protein dynamics during microvesicle exocytosis in neuroendocrine cells.Molecular biology of the cell · 2018Article
- How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018Review
- Fusion pores and their control of neurotransmitter and hormone release.The Journal of general physiology · 2017Review
- The Calcineurin-Binding, Activity-Dependent Splice Variant Dynamin1xb Is Highly Enriched in Synapses in Various Regions of the Central Nervous System.Frontiers in molecular neuroscience · 2017Article
- Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons.Frontiers in molecular neuroscience · 2017Review
- Imaging the recruitment and loss of proteins and lipids at single sites of calcium-triggered exocytosis.Molecular biology of the cell · 2016Article
- Small molecules demonstrate the role of dynamin as a bi-directional regulator of the exocytosis fusion pore and vesicle release.Molecular psychiatry · 2015Article
- Cell biology of yeast zygotes, from genesis to budding.Biochimica et biophysica acta · 2015Review
- Syndapin 3 modulates fusion pore expansion in mouse neuroendocrine chromaffin cells.American journal of physiology. Cell physiology · 2014Article
- Src kinases regulate de novo actin polymerization during exocytosis in neuroendocrine chromaffin cells.PloS one · 2014Article
- Dynamin-2 function and dysfunction along the secretory pathway.Frontiers in endocrinology · 2013Review
- Synaptic vesicle generation from activity-dependent bulk endosomes requires calcium and calcineurin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroendocrine chromaffin cells selectively secrete a variety of transmitter molecules into the circulation as a function of sympathetic activation. Activity-dependent release of transmitter species is controlled through regulation of the secretory fusion pore. Under sympathetic tone, basal synaptic excitation drives chromaffin cells to selectively secrete modest levels of catecholamine through a restricted secretory fusion pore. In contrast, elevated sympathetic activity, experienced under stress, results in fusion pore expansion to evoke maximal catecholamine release and to facilitate release of copackaged peptide transmitters. Therefore, fusion pore expansion is a key control point for the activation of the sympatho-adrenal stress response. Despite the physiological importance of this process, the molecular mechanism by which it is regulated remains unclear. Here we employ fluorescence imaging with electrophysiological and electrochemical-based approaches to investigate the role of dynamin I in the regulation of activity-mediated fusion pore expansion in mouse adrenal chromaffin cells. We show that under elevated stimulation, dynamin I is dephosphorylated at Ser-774 by calcineurin. We also demonstrate that disruption of dynamin I-syndapin binding, an association regulated by calcineurin-dependent dynamin dephosphorylation, limits fusion pore expansion. Last, we show that perturbation of N-WASP function (a syndapin substrate) limits activity-mediated fusion pore expansion. Our results suggest that fusion pore expansion is regulated by a calcineurin-dependent dephosphorylation of dynamin I. Dephosphorylated dynamin I acts via a syndapin/N-WASP signaling cascade to mediate pore expansion.
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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.