In many cell types, release of calcium ions is controlled by inositol 1,4,5-trisphosphate (IPxe2x82x83) receptor channels. Elevations in Caxc2xb2xe2x81xba concentration after intracellular release through IPxe2x82x83 receptors (IPxe2x82x83R) can either propagate in the form of waves spreading through the entire cell or produce spatially localized puffs. The appearance of waves and puffs is thought to implicate random initial openings of one or a few channels and subsequent activation of neighboring channels because of an autocatalytic feedback. It is much less clear, however, what determines the further time course of release, particularly since the lifetime is very different for waves (several seconds) and puffs (around 100 ms). Here we study the lifetime of Caxc2xb2xe2x81xba signals and their dependence on residual Caxc2xb2xe2x81xba microdomains. Our general idea is that Caxc2xb2xe2x81xba microdomains are dynamical and mediate the effect of other physiological processes. Specifically, we focus on the mechanism by which Caxc2xb2xe2x81xba binding proteins (buffers) alter the lifetime of Caxc2xb2xe2x81xba signals. We use stochastic simulations of channel gating coupled to a coarse-grained description for the Caxc2xb2xe2x81xba concentration. To describe the Caxc2xb2xe2x81xba concentration in a phenomenological way, we here introduce a differential equation, which reflects the buffer characteristics by a few effective parameters. This non-stationary model for microdomains gives deep insight into the dynamical differences between puffs and waves. It provides a novel explanation for the different lifetimes of puffs and waves and suggests that puffs are terminated by Caxc2xb2xe2x81xba inhibition while IPxe2x82x83 unbinding is responsible for termination of waves. Thus our analysis hints at an additional role of IP3 and shows how cells can make use of the full complexity in IPxe2x82x83R gating behavior to achieve different signals.