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.


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