Previous reports have shown that mechanically stimulated astrocytes release ATP.  In this review, we describe the mechanisms of an increase in intracellular Ca²⁺ concentration in stimulated astrocytes after receiving ATP in an autocrine fashion and those of intercellular communication among astrocytes by Ca²⁺ propagation.  We used astrocytes cultured from the cerebral cortices that were isolated from rat embryos.  First, we found two different Ca²⁺ pathways in stimulated astrocytes. ATP received by purine receptors in an autocrine fashion primarily activates a cascade including G-protein, phospholipase C and inositol-1,4,5-trisphosphate, resulting in intracellular Ca²⁺ mobilization.  The other Ca²⁺ system in astrocytes acts via a Ca²⁺ influx from the extracellular space.  Second, to elucidate a mechanism of ATP release from stimulated astrocytes, we analyzed the elasticity of astrocytes by atomic force microscopy. The most important contribution to the cell membrane elasticity comes from actin filaments, because the membrane above actin filaments is always stiffer than the surroundings.  A possible mechanism of ATP release in stimulated astrocytes may be, therefore, coupled to the deformation of actin filaments. Third, we analyzed the intercellular communication by Ca²⁺ propagation.  Colocalization of connexin and filamentous actin was observed in the regions of  cell-to-cell  adhesion  in  astrocytes.  Gap  junctional communication was also found to enable cell-to-cell coordination of actin filaments in astrocytes. This cell-to-cell coordination of actin filaments results in a widely spread intercellular communication by Ca²⁺ propagation.  In conclusion, actin filaments are strongly involved in intracellular and intercellular Ca²⁺ signaling in astrocytes.