Abstract
Elementary Ca2+ puffs form the basic building blocks of global Ins(1, 4,5)P3-evoked Ca2+ signals. In Xenopus oocytes, Ca2+ puffs evoked by the high-affinity agonist adenophostin were shorter and smaller than puffs evoked by Ins(1,4,5)P3 and the lower affinity analogue Ins(2,4, 5)P3. Agonist-specific mechanisms, therefore, play a role in shaping local Ca2+ release events, but termination of Ca2+ flux is not delimited simply by agonist dissociation.