Abstract
The platelet cytoplasm is filled with a network of actin filaments. The organization of these filaments is regulated by their association with proteins such as α-actinin, tropomyosin, and actin-binding protein (Fox, 1987). When platelets are activated, myosin associates with these cytoplasmic actin filaments, thus generating the tension required for the centralization of granules (Fox and Phillips, 1982; Painter and Ginsberg, 1984). New filaments are formed by the polymerization of monomeric actin (Carlsson et a1, 1979; Jennings et al, 1981); polymerization of these new filaments induces the extension of filopodia (Casella et al, 1981).