ArticleThe Journal of physiology2008
Discrete influx events refill depleted Ca2+ stores in a chick retinal neuron.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- Histamine elevates free intracellular calcium in mouse retinal dopaminergic cells via H1-receptors.Investigative ophthalmology & visual science · 2011Article
- Regulating survival and development in the retina: key roles for simple sphingolipids.Journal of lipid research · 2010Review
- Sphingosine-1-phosphate elicits receptor-dependent calcium signaling in retinal amacrine cells.Journal of neurophysiology · 2009Article
- Calcium homeostasis and cone signaling are regulated by interactions between calcium stores and plasma membrane ion channels.PloS one · 2009Article
- Depletion of calcium stores regulates calcium influx and signal transmission in rod photoreceptors.The Journal of physiology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The depletion of ER Ca2+ stores, following the release of Ca2+ during intracellular signalling, triggers the Ca2+ entry across the plasma membrane known as store-operated calcium entry (SOCE). We show here that brief, local [Ca2+]i increases (motes) in the thin dendrites of cultured retinal amacrine cells derived from chick embryos represent the Ca2+ entry events of SOCE and are initiated by sphingosine-1-phosphate (S1P), a sphingolipid with multiple cellular signalling roles. Externally applied S1P elicits motes but not through a G protein-coupled membrane receptor. The endogenous precursor to S1P, sphingosine, also elicits motes but its action is suppressed by dimethylsphingosine (DMS), an inhibitor of sphingosine phosphorylation. DMS also suppresses motes induced by store depletion and retards the refilling of depleted stores. These effects are reversed by exogenously applied S1P. In these neurons formation of S1P is a step in the SOCE pathway that promotes Ca2+ entry in the form of motes.
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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.