Abstract
Sphingosylphosphorylcholine (SPC) releases Ca2+ from brain microsomes. SPC-induced CA2+ release differs from IP3-induced Ca2+ release in that it is more extensive in the cerebrum than in the cerebellum. SPC has little effect on [3H] IP3 binding but enhances [3H] ryanodine binding, as expected for an activator of ryanodine receptors. SPC-induced Ca2+ release is inhibited by ryanodine receptor blockers but not by selective blockers of IP3 receptors. We conclude that SPC releases Ca2+ from brain microsomes by activating ryanodine receptors rather than IP3 receptors. Activation of an additional SPC-sensitive pathway for releasing Ca2+ is not precluded.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Brain / drug effects
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Brain / metabolism*
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Calcium / metabolism*
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Calcium Channels / physiology*
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Cattle
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Cerebellum / drug effects
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Cerebellum / metabolism
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Microsomes / metabolism
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Muscle Proteins / physiology*
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Palmitoyl Coenzyme A / pharmacology
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Phosphorylcholine / analogs & derivatives*
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Phosphorylcholine / pharmacology
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Quaternary Ammonium Compounds / pharmacology
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Ryanodine Receptor Calcium Release Channel
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Sphingosine / analogs & derivatives*
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Sphingosine / pharmacology
Substances
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Calcium Channels
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Muscle Proteins
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Quaternary Ammonium Compounds
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Ryanodine Receptor Calcium Release Channel
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sphingosine phosphorylcholine
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Phosphorylcholine
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Palmitoyl Coenzyme A
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tetrapentylammonium
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Sphingosine
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Calcium