Astrocytes are electrically non-excitable, and are incapable of electrochemical communication. Instead, the principle mechanism of astrocytic signaling involves transient elevations of cytosolic Ca2+ (Cotrina and Nedergaard, 2005). In light of the larger and more complex architecture of human astrocytes, we next asked whether propagation of intracellular Ca2+ signals in human astrocytes differs from that of rodents. To compare intracellular Ca2+ wave propagation between human and mouse astrocytes, we initiated localized Ca2+ increases by photolysis of caged Ca2+ (Parpura and Verkhratsky, 2011; Rusakov et al., 2011). Photolysis of caged Ca2 loaded specifically into astrocytes was used to avoid potentially confounding alterations in local synaptic activity. Intracellular Ca2+ waves were evoked by directing a UV beam at long processes of astrocytes filled with rhod-2 and NP-EGTA by a patch pipette. The subsequent spread of Ca2+ signals was visualized using 2-photon excitation (Fig. 3E). Line scanning with high temporal resolution (2-4 ms) showed that intracellular Ca2+ wave propagation was significantly faster in human astrocytes than murine cells; intracellular Ca2+ increases propagated with a velocity of 15.8 ± 0.7 μm/s among human glia, compared
