Sphingosylphosphorylcholine (SPC) induces a rapid increase of intracellular
Ca2+ concentration in isolated synaptosomes. This effect is dose-dependent
and is also dependent on extracellular Ca2+. Sphingosine (SPH) has a small
er effect and treatment with psychosine (PSY) is ineffective, which suggest
s that phosphorylation of the 1-carbon of SPH is required for the SPC to ac
t as a Ca2+ release agonist in synaptosomes. Experiments performed in the p
resence of heparin or ryanodine indicate that SPC-elicited Ca2+ release is
not mediated by IP3 or ryanodine receptors. Finally, our results show that
the effect of SPC on Ca2+ concentration is nimodipine-sensitive, suggesting
that SPC possibly activates a specific sphingolipid-gated Ca2+ channel in
synaptosomes.