Astrocytes express a complex repertoire of intracellular Ca transients (events) that represent a major form of signaling within individual cells and in astrocytic syncytium. These events have different spatiotemporal profiles, which are modulated by neuronal activity. Spontaneous Ca events appear more frequently in distal astrocytic processes and independently from each other. However, little is known about the mechanisms underlying such subcellular distribution of the Ca events. Here, we identify the initiation points of the Ca events within the territory of single astrocytes expressing genetically encoded Ca indicator GCaMP2 in culture or in hippocampal slices. We found that most of the Ca events start in an optimal range of thin distal processes. Our mathematical model demonstrated that a high surface-to-volume of the thin processes leads to increased amplitude of baseline Ca fluctuations caused by a stochastic opening of Ca channels in the plasma membrane. Suprathreshold fluctuations trigger Ca -induced Ca release from the Ca stores by activating inositol 1,4,5-trisphosphate (IP ) receptors. In agreement with the model prediction, the spontaneous Ca events frequency depended on the extracellular Ca concentration. Astrocytic depolarization by high extracellular K increased the frequency of the Ca events through activation of voltage-gated Ca channels in cultured astrocytes. Our results suggest that the morphological profile of the astrocytic processes is responsible for tuning of the Ca events frequency. Therefore, structural plasticity of astrocytic processes can be directly translated into changes in astrocytic Ca signaling. This may be important for both physiological and pathological astrocyte remodeling.