Nicotinic acid adenine dinucleotide phosphate-induced Ca²⁺ release. Interactions among distinct Ca²⁺ mobilizing mechanisms in starfish oocytes

An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP⁺) contributes to intracellular Ca²⁺ release alongside inositol 1,4,5-trisphosphate (Ins-P₃) and ryanodine receptors. The NAADP⁺-sensitive mechanism has been shown to be operative in sea urchin eggs, ascidian eggs, and pancreatic acinar cells. Furthermore, most mammalian cell types can synthesize NAADP⁺, with nicotinic acid and NADP⁺ as precursors. In this contribution, NAADP⁺ induced Ca²⁺ release has been investigated in starfish oocytes. Uncaging of injected NAADP⁺ induced Ca²⁺ mobilization in both immature oocytes and in oocytes matured by the hormone 1-methyladenine (1-MA). The role of extracellular Ca²⁺ in NAADP⁺-induced Ca²⁺ mobilization, which was minor in immature oocytes, was instead essential in mature oocytes. Thus, the NAADP⁺sensitive Ca²⁺ pool, which is known to be distinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPribose, apparently migrated closer to (or became part of) the plasma membrane during the maturation process. Inhibition of both Ins-P₃ and ryanodine receptors, but not of either alone, substantially inhibited NAADP⁺-induced Ca²⁺ mobilization in both immature and mature oocytes. The data also suggest that NAADP⁺-induced Ca²⁺ mobilization acted as a trigger for Ca²⁺ release via Ins-P₃ and ryanodine receptors.