Role of inositol lipid degradation

Ca2+ levels, with one of the intracellular calcium-chelating, fluorescent probes, quin-2, fura-2 or indo-1, demonstrates that, in both cases, there is a rapid rise in intracellular Ca2+ as this ion is released from intracellular stores. Analysis of stimulated B lymphocytes, using the probe fura-2, indicates that if Ca2+ in the external medium is removed the intracellular Ca2+ level returns to basal levels in 5 to 7 minutes, but if there is Ca2+ present in the external media a sustained increase in intracellular Ca2+ is detected [36]. Such analysis suggests the opening of a plasma membrane calcium channel but the nature of the channel or mechanism of its opening are not presently known. It is possible that the opening of this channel could be stimulated by one of the inositol phosphates. 

The increase in phosphoinositide hydrolysis appears to occur during the G0 and early G[ phases of the cell cycle. Cells will not tolerate a sustained increase in intracellular Ca2+ and actively extrude the ion. Recent evidence in B lymphocytes, using calcium probes and image intensifies, shows that when surface immunoglobulin is crosslinked the rise of intracellular Ca2+ occurs in repeated short bursts [37]. 

Influence of ionophores and synthetic stimulators of protein kinase C 

The enzymatic reactions associated with the generation of these multiple activating pathways based on the inositol phospholipids may represent the site of action of 

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