Calcium-induced calcium release (CICR) is an inherently regenerative process due 
to the Ca(2+)-dependent gating of ryanodine receptors (RyRs) in the 
sarco/endoplasmic reticulum (SR) and is critical for cardiac 
excitation-contraction coupling. This process is seen as Ca(2+) sparks, which 
reflect the concerted gating of groups of RyRs in the dyad, a specialised 
junctional signalling domain between the SR and surface membrane. However, the 
mechanism(s) responsible for the termination of regenerative CICR during the 
evolution of Ca(2+) sparks remain uncertain. Rat cardiac RyR gating was recorded 
at physiological Ca(2+), Mg(2+) and ATP levels and incorporated into a 3D model 
of the cardiac dyad which reproduced the time-course of Ca(2+) sparks, Ca(2+) 
blinks and Ca(2+) spark restitution. Model CICR termination was robust, 
relatively insensitive to the number of dyadic RyRs and automatic. This emergent 
behaviour arose from the rapid development and dissolution of nanoscopic Ca(2+) 
gradients within the dyad. These simulations show that CICR does not require 
intrinsic inactivation or SR calcium sensing mechanisms for stability and 
cessation of regeneration that arises from local control at the molecular scale 
via a process we call 'induction decay'.