Extracellular ATP plays important roles in coordinating the activities of astrocytes and neurons, and aberrant signalling is associated with neurodegenerative diseases. In rodents, ATP stimulates opening of Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$-permeable channels formed by P2X receptor subunits in the plasma membrane. It is widely assumed, but not verified, that P2X receptors also evoke Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$ signals in human astrocytes. Here we directly assess this hypothesis. We showed that cultured foetal cortical human astrocytes express mRNA for several P2X receptor subunits (P2X$4$, P2X$5$, P2X$6$) and G-protein-coupled P2Y receptors (P2Y$1$, P2Y$2$, P2Y$6$, P2Y$\mathrm{<mrow\; data-mjx-texclass="ORD">11</mrow>}$). In these astrocytes, ATP stimulated Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$ release from intracellular stores through IP$3$ receptors and store-operated Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$ entry. These responses were entirely mediated by P2Y$1$ and P2Y$2$ receptors. Agonists of P2X receptors did not evoke Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$ signals, and nor did ATP when Ca$\mathrm{<mrow\; data-mjx-texclass="ORD">2+</mrow>}$ release from intracellular stores and store-operated $\mathrm{<mrow\; data-mjx-texclass="ORD"></mrow>}$Ca$^{}$2+entrywereinhibited.WeconcludethatATP-evokedCa$^{2+}$ signals in cultured human foetal astrocytes are entirely mediated by P2Y$1$ and P2Y$2$ receptors, with no contribution from P2X receptors.