An intracellular mechanism activated by nicotinic acid adenine dinucleotide
phosphate (NAADP(+)) contributes to intracellular Ca2+ release alongside i
nositol 1,4,5-trisphosphate (Ins-P-3) and ryanodine receptors. The NAADP(+)
-sensitive mechanism has been shown to be operative in sea urchin eggs, asc
idian eggs, and pancreatic acinar cells. Furthermore, most mammalian cell t
ypes 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+ mobilizati
on in both immature oocytes and in oocytes matured by the hormone 1-methyla
denine (1-MA), The role of extracellular Ca2+ in NAADP(+)-induced Ca2+ mobi
lization, which was minor in immature oocytes, was instead essential in mat
ure oocytes, Thus, the NAADP(+)-sensitive Ca2+ pool, which is known to be d
istinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPr
ibose, apparently migrated closer to (or became part of) the plasma membran
e during the maturation process. Inhibition of both Ins-P-3 and ryanodine r
eceptors, but not of either alone, substantially inhibited NAADP(+)-induced
Ca2+ mobilization in both immature and mature oocytes. The data also sugge
st that NAADP(+)-induced Ca2+ mobilization acted as a trigger for Ca2+ rele
ase via Ins-P-3 and ryanodine receptors.