The role of calcium stores in cytoplasmic calcium signal termination was studied in acutely isolated small and large DRG neurones from mice. Cytoplasmic calcium concentration ([Ca2+]in) was recorded using indo-1 microfluorometry and membrane potential was monitored by 'perforated' whole-cell patch-clamp. Depolarization-induced [Ca2+]in transients recovered significantly faster in large neurones than in small neurones. Caffeine was able to release Ca2+ from internal stores only in large neurones, while small neurones lacked caffeine-releasable calcium stores. Thapsigargin abolished caffeine-induced Ca2+ release and significantly slowed down recovery of depolarization-triggered [Ca2+]in transients in large neurones. We conclude that [Ca2+]in signals recover faster in large DRG neurones, at least in part due to the higher rate of Ca2+ sequestration by intracellular stores.