ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Influence of cholesterol on catecholamine release from the fusion pore of large dense core chromaffin granules.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 49 citations in OpenAlex.
- Three membrane fusion pore families determine the pathway to pore dilation.Biophysical journal · 2023Article
- Requirement of Cholesterol for Calcium-Dependent Vesicle Fusion by Strengthening Synaptotagmin-1-Induced Membrane Bending.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Drunken lipid membranes, not drunken SNARE proteins, promote fusion in a model of neurotransmitter release.Frontiers in molecular neuroscience · 2022Article
- Sterols lower energetic barriers of membrane bending and fission necessary for efficient clathrin-mediated endocytosis.Cell reports · 2021Article
- Cholesterol stabilizes recombinant exocytic fusion pores by altering membrane bending rigidity.Biophysical journal · 2021Article
- How proteins open fusion pores: insights from molecular simulations.European biophysics journal : EBJ · 2021Review
- Exocytotic fusion pore under stress.Cell stress · 2020Review
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Fusion pores and their control of neurotransmitter and hormone release.The Journal of general physiology · 2017Review
- The role of cholesterol in membrane fusion.Chemistry and physics of lipids · 2016Review
- Cholesterol Increases the Openness of SNARE-Mediated Flickering Fusion Pores.Biophysical journal · 2016Article
- Variations in Fusion Pore Formation in Cholesterol-Treated Platelets.Biophysical journal · 2016Article
- Free energy landscape of rim-pore expansion in membrane fusion.Biophysical journal · 2014Article
- Characterisation of Weibel-Palade body fusion by amperometry in endothelial cells reveals fusion pore dynamics and the effect of cholesterol on exocytosis.Journal of cell science · 2013Article
- Phospholipid scramblase-1-induced lipid reorganization regulates compensatory endocytosis in neuroendocrine cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Influence of cholesterol on cellular signaling and fusion pore kinetics.Journal of molecular neuroscience : MN · 2012Review
- Article
- A new approach to the molecular analysis of docking, priming, and regulated membrane fusion.Journal of chemical biology · 2011Article
- Chemical analysis of single cells.Analytical chemistry · 2011Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Changes in cellular cholesterol can affect exocytosis, but the influence of cholesterol in fusion pore kinetics is unclear. Using carbon fiber amperometry, we monitored quantal catecholamine release from rat chromaffin cells. To bypass any possible effect of cholesterol perturbation on ion channels or the colocalization of voltage-gated Ca(2+) channels with sites of exocytosis, exocytosis was stimulated via uniform elevation of cytosolic [Ca(2+)] (with whole-cell dialysis of a Ca(2+)-buffered solution). Under this condition, alterations of cellular cholesterol affected neither the mean number of amperometric events triggered per cell nor their quantal size and the kinetics of their main spike (which reflects the rapid release during and after rapid fusion pore dilation). In contrast, the reduction of cellular cholesterol shortened the "prespike foot" signals (which reflect the leakage of catecholamine via a semi-stable fusion pore) and reduced the proportion of "stand-alone foot" signals (which reflect the release via a flickering fusion pore that may close before it dilates significantly), whereas an oversupply of cholesterol had opposite effects. Acute extraction of cholesterol from the cytosol (via whole-cell dialysis of a cholesterol extractor) also shortened the prespike foot signals and reduced the proportion of stand-alone foot signals, but acute extracellular application of cholesterol extractor or "soluble" cholesterol had no effect. Our data raise the possibility that cholesterol molecules, particularly those in the cytoplasmic leaflet, helps to constrain the narrow waistline of a semi-stable fusion pore while it is flickering or before it starts to dilate rapidly.
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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 OpenQuestion graph.