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Sphingosylphosphorylcholine increases calcium concentration in isolated brain nuclei
M C Calcerrada1, B G Miguel, R E Catalan
1Departamento de Biologia Molecular, Centro de Biologia Molecular Severo Ochoa (CSIC-UAM), Universidad Autónoma de Madrid, Spain.
Neuroscience Research
|April 22, 1999
Summary
Sphingosylphosphorylcholine (SPC) rapidly increases calcium in brain nuclei. This calcium increase is blocked by L-type calcium channel inhibitors and Ca2+-ATPase inhibitors, but not by phospholipase C or protein kinase C pathways.
Area of Science:
- Neuroscience
- Cellular Biology
- Biochemistry
Background:
- Sphingolipids play crucial roles in cellular signaling.
- Sphingosylphosphorylcholine (SPC) is a bioactive sphingolipid with known cellular effects.
- Calcium signaling is fundamental to neuronal function.
Purpose of the Study:
- To investigate the mechanism by which SPC affects intracellular calcium concentration in isolated brain nuclei.
- To determine the specific ion channels and signaling pathways involved in SPC-induced calcium changes.
Main Methods:
- Measurement of intracellular calcium concentration in isolated brain nuclei.
- Application of SPC and various inhibitors (nimodipine, thapsigargin, heparin, U73122).
- Assessment of protein kinase C activity.
Main Results:
- SPC induced a rapid and significant increase in Ca2+ concentration in isolated brain nuclei.
- Nimodipine (L-type Ca2+ channel inhibitor) and thapsigargin (Ca2+-ATPase inhibitor) blocked the SPC-induced Ca2+ increase.
- Heparin and U73122 did not affect the SPC-induced Ca2+ increase, indicating no involvement of phospholipase C or IP3.
- The SPC effect was independent of protein kinase C.
Conclusions:
- SPC-mediated calcium increase in brain nuclei involves L-type calcium channels and Ca2+-ATPase.
- The mechanism does not rely on phospholipase C/IP3 or protein kinase C signaling pathways.
- SPC is a potent modulator of calcium homeostasis in neuronal nuclei.