Astroglia possess excitability based on movements of Ca(2+) ions between intracellular compartments and plasmalemmal Ca(2+) fluxes. This "Ca(2+) excitability" is controlled by several families of proteins located in the plasma membrane, within the cytosol and in the intracellular organelles, most notably in the endoplasmic reticulum (ER) and mitochondria. Accumulation of cytosolic Ca(2+) can be caused by the entry of Ca(2+) from the extracellular space through ionotropic receptors and store-operated channels expressed in astrocytes. Plasmalemmal Ca(2+) ATP-ase and sodium-calcium exchanger extrude cytosolic Ca(2+) to the extracellular space; the exchanger can also operate in reverse, depending of the intercellular Na(+) concentration, to deliver Ca(2+) to the cytosol. The ER internal store possesses inositol 1,4,5-trisphosphate receptors which can be activated upon stimulation of astrocytes through a multiple plasma membrane metabotropic G-protein coupled receptors. This leads to release of Ca(2+) from the ER and its elevation in the cytosol, the level of which can be modulated by mitochondria. The mitochondrial uniporter takes up Ca(2+) into the matrix, while free Ca(2+) exits the matrix through the mitochondrial Na(+)/Ca(2+) exchanger as well as via transient openings of the mitochondrial permeability transition pore. One of the prominent consequences of astroglial Ca(2+) excitability is gliotransmission, a release of transmitters from astroglia which can lead to signalling to adjacent neurones.