Sphingosylphosphorylcholine increases calcium concentration in isolated brain nuclei

Sphingosylphosphorylcholine (SPC) caused a rapid increase of Ca 2+ concentration in isolated brain nuclei. This effect was prevented by nimodipine, an inhibitor of L-type Ca 2+ channels, and by thapsigargin, an inhibitor of Ca 2+-ATPase. Neither heparin nor U73122 modified this effect, suggesting th...

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Bibliographic Details
Published in:Neuroscience research 1999-03, Vol.33 (3), p.229-232
Main Authors: Calcerrada, M.C., Miguel, B.G., Catalan, R.E., Martinez, A.M.
Format: Article
Language:English
Subjects:
Animals
Brain
Brain - drug effects
Brain - metabolism
Calcium
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium-Transporting ATPases - antagonists & inhibitors
Cell Nucleus - drug effects
Cell Nucleus - metabolism
Estrenes - pharmacology
Heparin - pharmacology
In Vitro Techniques
Kinetics
Nimodipine
Nimodipine - pharmacology
Nucleus
Phosphorylcholine - analogs & derivatives
Phosphorylcholine - pharmacology
Protein kinase C
Pyrrolidinones - pharmacology
Rats
Sphingosine - analogs & derivatives
Sphingosine - pharmacology
Sphingosylphosphorylcholine
Thapsigargin - pharmacology
Type C Phospholipases - antagonists & inhibitors
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Summary:Sphingosylphosphorylcholine (SPC) caused a rapid increase of Ca 2+ concentration in isolated brain nuclei. This effect was prevented by nimodipine, an inhibitor of L-type Ca 2+ channels, and by thapsigargin, an inhibitor of Ca 2+-ATPase. Neither heparin nor U73122 modified this effect, suggesting that phospholipase C activation and inositol 1,4,5-trisphosphate (IP 3) production are not involved. Results also indicated that SPC-induced increase in Ca 2+ concentration is not protein kinase C-dependent.
ISSN:0168-0102
1872-8111
DOI:10.1016/S0168-0102(99)00004-8