1) Membrane currents were recorded under voltage-clamp from cells using patch-clamp pipettes. Cells were dialysed with potassium-free caesium solution to block any Ca-activated K-current. The pipette solution contained Indo-1 and the ratio of the emissions from this dye at 480 and 405 nm was used to estimate the free calcium concentration in the cell. 2) Carbachol applied to the cell evoked at -50 mV an initial increase in the intracellular calcium concentration (Cai) followed by a smaller sustained rise (plateau); the changes in inward cationic current (ICarb) closely followed changes in Cai. Calcium entry blockers did not affect these responses. 3) The initial peak in Cai produced by carbachol was due to calcium store release: it was present in calcium-free solution, and unchanged at +50 mV, but it was abolished by prior application of caffeine (10 mM) to the cell or by inclusion of heparin (which blocks D-myoinositol 1,4,5-trisphosphate receptors) in the pipette. 4) The sustained rise (plateau) in Cai produced by carbachol was due to the entry of calcium into the cell down its electrochemical gradient as it was affected by changing the cell membrane potential or the calcium concentration in the bathing solution. As the sustained rise in Cai produced by caffeine had similar properties it was suggested that depletion of calcium stores can evoke an increased calcium entry into the cell through some pathway.