Ca$^2+$ ions passing through a single or a cluster of Ca$^2+$-permeable
channels create microscopic, short-lived Ca$^2+$ gradients that
constitute the building blocks of cellular Ca$^2+$ signaling.
Over the last decade, imaging microdomain Ca$^2+$ in muscle cells
has unveiled the exquisite spatial and temporal architecture of intracellular
Ca$^2+$ dynamics and has reshaped our understanding of Ca$^2+$
signaling mechanisms. Major advances include the visualization of
"Ca$^2+$ sparks" as the elementary events of Ca$^2+$ release
from the sarcoplasmic reticulum (SR), "Ca$^2+$ sparklets" produced
by openings of single Ca$^2+$-permeable channels, miniature Ca$^2+$
transients in single mitochondria ("marks"), and SR luminal Ca$^2+$
depletion transients ("scraps"). As a model system, a cardiac myocyte
contains a 3-dimensional grid of 104 spark ignition sites, stochastic
activation of which summates into global Ca$^2+$ transients.
Tracking intermolecular coupling between single L-type Ca$^2+$
channels and Ca$^2+$ sparks has provided direct evidence validating
the local control theory of Ca$^2+$-induced Ca$^2+$ release
in the heart. In vascular smooth muscle myocytes, Ca$^2+$ can
paradoxically signal both vessel constriction (by global Ca$^2+$
transients) and relaxation (by subsurface Ca$^2+$ sparks). These
findings shed new light on the origin of Ca$^2+$ signaling efficiency,
specificity, and versatility. In addition, microdomain Ca$^2+$
imaging offers a novel modality that complements electrophysiological
approaches in characterizing Ca$^2+$ channels in intact cells.