The past three years have seen significant advances in our knowledge and understanding of Ca2+ mobilization in platelets. Some of the data has shown that systems demonstrated in other cell types operate in platelets, while in certain respects platelet studies have provided the lead with new insights and approaches. An increasing body of evidence supports a key role for Ins1,4,5-trisphosphate in mediating internal release, but it has yet to be experimentally demonstrated that this messenger is formed fast enough to account for the observed kinetics of internal release that can reach its maximum rate within 250 msec. There also remains a question as to the presence of an alternative or additional pathway linking at least ADP receptors to internal Ca2+ release. The controversy over the role of pHi in Ca2+ mobilization appears to be resolved; changes in pHi are neither sufficient nor necessary but can modulate the process in some instances. Elevated cAMP and protein kinase C inhibit Ca mobilization, but the sites and mechanisms of action are not worked out. Analysis of receptor-mediated Ca2+ entry by stopped-flow fluorescence has increasingly revealed a complex array of mechanisms, but there is no evidence for voltage-gated Ca2+ entry. There are indications of at least three pathways: a fast entry closely coupled to the ADP receptor; a process that may be generated by a diffusible second messenger, possibly an inositol phosphate; and an entry regulated by the state of filling of the discharged Ca2+ store. A recent advance has been the successful application of the patch-clamp to these tiny cells, with evidence for voltage-gated K+ channels and ADP-stimulated single channels that could be the pathway for the fast phase of ADP-evoked [Ca2+]i elevation.