ArticleProceedings of the National Academy of Sciences of the United States of America2005
Ca2+ sparks and secretion in dorsal root ganglion neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
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- TRPA1-dependent calcium transients and CGRP release in DRG neurons require extracellular calcium.The Journal of cell biology · 2020Article
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- Advanced oxidation protein products sensitized the transient receptor potential vanilloid 1 via NADPH oxidase 1 and 4 to cause mechanical hyperalgesia.Redox biology · 2016Article
- Functional ryanodine receptors in the membranes of neurohypophysial secretory granules.The Journal of general physiology · 2014Article
- Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy.The journal of pain · 2013Article
- Ryanodine Receptors Selectively Interact with L Type Calcium Channels in Mouse Taste Cells.PloS one · 2013Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Ca(2+) sparks as the elementary intracellular Ca(2+) release events are instrumental to local control of Ca(2+) signaling in many types of cells. Here, we visualized neural Ca(2+) sparks in dorsal root ganglion (DRG) sensory neurons and investigated possible role of DRG sparks in the regulation of secretion from the somata of the cell. DRG sparks arose mainly from type 3 ryanodine receptor Ca(2+) release channels on subsurface cisternae of the endoplasmic reticulum, rendering a striking subsurface localization. Caffeine- or 3,7-dimethyl-1-(2-propynyl)xanthine-induced store Ca(2+) release, in the form of Ca(2+) sparks, triggered exocytosis, independently of membrane depolarization and external Ca(2+). The spark-secretion coupling probability was estimated to be between 1 vesicle per 6.6 sparks and 1 vesicle per 11.4 sparks. During excitation, subsurface sparks were evoked by physiological Ca(2+) entry via the Ca(2+)-induced Ca(2+) release mechanism, and their synergistic interaction with Ca(2+) influx accounted for approximately 60% of the Ca(2+)-dependent exocytosis. Furthermore, inhibition of Ca(2+)-induced Ca(2+) release abolished endotoxin-induced secretion of pain-related neuropeptides. These findings underscore an important role for Ca(2+) sparks in the amplification of surface Ca(2+) influx and regulation of neural secretion.
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