ArticleThe Journal of biological chemistry2010
Conformational changes induced in voltage-gated calcium channel Cav1.2 by BayK 8644 or FPL64176 modify the kinetics of secretion independently of Ca2+ influx.
Article in The Journal of biological chemistry, 2010. 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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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- Calcium Channel Blockers Inhibit Pancreatic Neuroendocrine Neoplasms Progression via Cav1.2-Epigenetic Circuit.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Non-ionotropic voltage-gated calcium channel signaling.Channels (Austin, Tex.) · 2024Review
- Clustering of CaJournal of neurochemistry · 2023Article
- Antispasmodic effects of the essential oil ofHeliyon · 2020Article
- The physiology of regulated BDNF release.Cell and tissue research · 2020Review
- Relaxant Effect of Monoterpene (-)-Carveol on Isolated Human Umbilical Cord Arteries and the Involvement of Ion Channels.Molecules (Basel, Switzerland) · 2020Article
- β-Subunit of the voltage-gated CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Hydroxyl Group and Vasorelaxant Effects of Perillyl Alcohol, Carveol, Limonene on Aorta Smooth Muscle of Rats.Molecules (Basel, Switzerland) · 2018Article
- Intra-membrane signaling between the voltage-gated Ca2+-channel and cysteine residues of syntaxin 1A coordinates synchronous release.Scientific reports · 2013Article
- Control of depolarization-evoked presynaptic neurotransmitter release by Cav2.1 calcium channel: old story, new insights.Channels (Austin, Tex.)Article
- Properties of Na+ currents conducted by a skeletal muscle L-type Ca2+ channel pore mutant (SkEIIIK).Channels (Austin, Tex.)Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the L-type calcium channel (Cav1.2) as a molecular switch that triggers secretion prior to Ca(2+) transport has previously been demonstrated in bovine chromaffin cells and rat pancreatic beta cells. Here, we examined the effect of specific Cav1.2 allosteric modulators, BayK 8644 (BayK) and FPL64176 (FPL), on the kinetics of catecholamine release, as monitored by amperometry in single bovine chromaffin cells. We show that 2 microm BayK or 0.5 microm FPL accelerates the rate of catecholamine secretion to a similar extent in the presence either of the permeable Ca(2+) and Ba(2+) or the impermeable charge carrier La(3+). These results suggest that structural rearrangements generated through the binding of BayK or FPL, by altering the channel activity, could affect depolarization-evoked secretion prior to cation transport. FPL also accelerated the rate of secretion mediated by a Ca(2+)-impermeable channel made by replacing the wild type alpha(1)1.2 subunit was replaced with the mutant alpha(1)1.2/L775P. Furthermore, BayK and FPL modified the kinetic parameters of the fusion pore formation, which represent the initial contact between the vesicle lumen and the extracellular medium. A direct link between the channel activity and evoked secretion lends additional support to the view that the voltage-gated Ca(2+) channels act as a signaling molecular switch, triggering secretion upstream to ion transport into the cell.
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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.