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M300212200v1
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Papers In Press, published online ahead of print April 22, 2003
J. Biol. Chem, 10.1074/jbc.M300212200
Submitted on January 8, 2003
Revised on April 14, 2003
Accepted on April 22, 2003

Glucosylceramide and glucosylsphingosine modulate calcium mobilizationfrom brain microsomes via different mechanisms

Emyr Lloyd-Evans, Dori Pelled, Christian Riebeling, Jacques Bodennec, Aviv de-Morgan, Helen Waller, Raphael Schiffmann, and Anthony H. Futerman

Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100

Corresponding Author: tony.futerman{at}weizmann.ac.il

We recently demonstrated that elevation of intracellular glucosylceramide (GlcCer) levels results in increased functional Ca2+ stores in cultured neurons, and suggested that this may be due to modulation of ryanodine receptors (RyaRs) by GlcCer (Korkotian, E., Schwarz, A., Pelled, D., Schwarzmann, G., Segal, M. and Futerman, A.H. J. Biol. Chem. 274, 21673-21678). We now systematically examine the effects of exogenously added GlcCer, other glycosphingolipids (GSLs) and their lyso-derivatives on Ca2+-release from rat brain microsomes. GlcCer had no direct effect on Ca2+-release, but rather augmented agonist-stimulated Ca2+-release via RyaRs, through a mechanism that may involve the redox sensor of the RyaR, but had no effect on Ca2+-release via inositol 1,4,5-trisphosphate receptors. Other GSLs and sphingolipids, including galactosylceramide, lactosylceramide, ceramide, sphingomyelin, sphingosine-1-phosphate, sphinganine-1-phosphate and sphingosylphosphorylcholine had no effect on Ca2+-mobilization from rat brain microsomes, but both galactosylsphingosine (psychosine) and glucosylsphingosine stimulated Ca2+-release, although only galactosylsphingosine mediated Ca2+-release via the RyaR. Finally, we demonstrated that GlcCer levels were ~10-fold higher in microsomes prepared from the temporal lobe of a type 2 Gaucher disease patient compared to a control, and Ca2+-release via the RyaR was significantly elevated, which may be of relevance for explaining the pathophysiology of neuronopathic forms of Gaucher disease.


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