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Ca2+currents) is smal-ler during the uptake by Ca2+pumps than at the rapid releasephase through InsP3receptor channels. The increase in the membrane resistance of Ca2+store mayindicate closures of some ionic channels in the membrane ofCa2+store. In fact, voltage- and Ca2+-activated potassium(BK-type) channels are present in the nuclear envelope or per-inuclear ER [32,33]. The store BK channel is activated by po-sitive shifts in the luminal potential and luminal Ca2+increases[32,33]. From these properties of the store BK channel and thedynamics of the membrane potential of Ca2+store, ‘luminalpotential’ model has been proposed to account for ‘quantal’Ca2+release.
Adenophostin-medicated quantal Ca2+ release in the purified and reconstituted inositol 1, 4, 5-trisphosphate receptor type 1.
Such a graded release seems, at first sight, incompatible both with the finite capacity of the store and the positive feedback CICR-like facility at Ins(1,4,5)P3Rs (Iino, 1990) that, once activated, would be anticipated to release the entire SR Ca2+ content. Yet Ca2+ release from the SR by means of Ins(1,4,5)P3Rs is both controlled and graded by the concentration of Ins(1,4,5)P3 (Meyer and Stryer, 1990). This process of graded Ca2+ release through Ins(1,4,5)P3Rs has been termed `quantal' (Muallem et al. , 1989), initially to imply an all-or-none release of discrete Ca2+ pools, analogous to events involving acetylcholine at the skeletal neuromuscular junction (Fatt and Katz, 1952). The term `quantal' release.
The release of intracellular Ca2+ is characterised by a graded response when submaximal doses of agonists are used. The basic phenomenon, called “quantal Ca2+ release”, is that even the maintained presence of a submaximal dose of agonist or of InsP3 for long time periods (up to 20 min) provokes only a partial release of Ca2+. This partial, or quantal, release phenomenon is due to the fact that the initially very rapid InsP3-induced Ca2+ release eventually develops into a much slower release phase.