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Sphingolipid derivatives modulate intracellular Ca2+ in rat synaptosomes
B G Miguel1, M C Calcerrada, R E Catalán
1Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Complutense University, E-28040 Madrid, Spain.
Acta Neurobiologiae Experimentalis
|August 22, 2001
Summary
Sphingosylphosphorylcholine (SPC) rapidly increases intracellular calcium (Ca2+) in synaptosomes, requiring extracellular Ca2+. This effect suggests SPC activates a novel sphingolipid-gated calcium channel.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Sphingolipids play crucial roles in cellular signaling.
- Calcium ions (Ca2+) are vital for neurotransmission and synaptic function.
Purpose of the Study:
- To investigate the effect of sphingosylphosphorylcholine (SPC) on intracellular Ca2+ concentration in isolated synaptosomes.
- To elucidate the mechanism of SPC-induced Ca2+ release and identify potential ion channels involved.
Main Methods:
- Measurement of intracellular Ca2+ concentration in isolated synaptosomes.
- Dose-response studies with SPC, sphingosine (SPH), and psychosine (PSY).
- Experiments using heparin, ryanodine, and nimodipine to probe signaling pathways.
Main Results:
- SPC induced a rapid, dose-dependent, and extracellular Ca2+-dependent increase in intracellular Ca2+.
- SPH showed a minor effect, while PSY was ineffective, indicating the necessity of SPC's phosphorylated form.
- SPC-induced Ca2+ release was independent of IP3 and ryanodine receptors but sensitive to nimodipine.
Conclusions:
- Phosphorylation of sphingosine is essential for Ca2+ release in synaptosomes.
- SPC likely activates a novel sphingolipid-gated Ca2+ channel, distinct from IP3 and ryanodine receptors.
- The nimodipine sensitivity suggests a role for L-type calcium channels or associated proteins in SPC signaling.