Occupation of membrane receptors can evoke calcium signals by causing depolarisation and activating voltage-operated calcium channels, by triggering internal release, or by stimulating calcium influx processes not gated by membrane potential, receptor-mediated calcium entry, RCME. This brief review considers different possible coupling mechanisms and the proposal that entry can occur from external medium to intracellular store, by-passing the cytosol, and regulated by the state of filling of the store. Recent studies using Mn2+ as a probe for RCME are outlined, as are some new electrophysiologic measurements with human platelets and investigations of a novel blocker of RMCE, SK&F 96365.