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Fertilization of the mammalian egg initiates transient and repetitive release of Ca2+ from intracellular stores. The mechanism by which these Ca2+ transients are produced is not completely known. We examined the role of two principal Ca2+ release mechanisms, inositol trisphosphate-induced Ca2+ release and Ca(2+)-induced Ca2+ release, in altering intracellular Ca2+ in the mouse egg. Microinjection of inositol 1,4,5-trisphosphate (IP3) transiently elevated intracellular Ca2+ and, at higher concentrations, produced repetitive Ca2+ transients. Addition of 100 microM thimerosal, a sulfhydryl reagent, caused repetitive Ca2+ transients. IP3 and thimerosal responses were inhibited by prior injection of heparin, a competitive antagonist of IP3-induced Ca2+ release. Addition of caffeine or injection of caffeine, ryanodine, or cyclic ADP-ribose, which are known to initiate or modulate Ca(2+)-induced Ca2+ release in sea urchin eggs and other cells, produced no change in intracellular Ca2+. The response to injection of Ca2+ was not altered by prior injection of ryanodine. The magnitude of the Ca2+ transients produced by injection of IP3 was not changed by prior injection of cyclic ADP-ribose or external caffeine. We found no evidence of Ca(2+)-induced Ca2+ release from ryanodine- or caffeine-sensitive stores. It is most likely that release of Ca2+ from intracellular stores in the mouse egg is dependent on IP3-induced Ca2+ release.

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