The endothelin (ET) isoforms ET-1, ET-2 and ET-3 applied at 100 nM triggered a transient increase in Ca 2+ i in Bergmann glial cells in cerebellar slices acutely isolated from 20–25 day-old mice. The intracellular calcium concentration (Ca 2+ i) was monitored using Fura-2-based (Ca 2+ i) microfluorimetry. The ET-triggered (Ca 2+ i) transients were mimicked by ET, receptor agonist BO-3020 and were inhibited by ETB receptor antagonist BQ-788. ET elevated Ca 2+ i in Ca2+-free extracellular solution and the ET-triggered Ca 2+ i elevation was blocked by 500 nM thapsigargin indicating that the Ca 2+ i was released from InsP3 sensitive intracellular pools. The ET-triggered Ca 2+ i increase in Ca 2+-free solution was shorter in duration. Restoration of normal extracellular Ca 2+ briefly after the ET application induced a second Ca 2+ i increase indicating the presence of a secondary Ca 2+ influx which prolongs the Ca 2+ signal. Pre-application of 100 μM ATP or 10 μM noradrenaline blocked the ET response suggesting the involvement of a common Ca 2+ depot. The expression of ETB receptor mRNAs in Bergmann glial cells was revealed by single-cell RT-PCR. The mRNA was also found in Purkinje neurones, but no Ca 2+ signalling was triggered by ET. We conclude that Bergmann glial cells are endowed with functional ET B receptors which induce the generation of intracellular Ca 2+ i signals by activation of Ca 2+ release from InsP 3-sensitive intracellular stores followed by a secondary Ca 2+ influx.