Astrocytes express a plethora of ion channels, neurotransmitter receptors and transporters and thus are endowed with the machinery to sense and respond to neuronal activity. Recent studies have implicated astrocytes in important physiological roles in the CNS, such as synchronization of neuronal firing, ion homeostasis, neurotransmitter uptake, glucose metabolism and regulation of the vascular tone. Astrocytes are abundantly coupled through gap junctions allowing them to redistribute elevated K⁺ concentration from sites of excessive neuronal activity. Growing evidence now suggests that dysfunctional astrocytes are crucial players in epilepsy. Investigation of specimens from patients with pharmacoresistant temporal lobe epilepsy and epilepsy models revealed alterations in expression, localization and function of astroglial K⁺ and water channels, entailing impaired K⁺ buffering. Moreover, malfunction of glutamate transporters and the astrocytic glutamate-converting enzyme, glutamine synthetase, as observed in epileptic tissue suggested that astrocyte dysfunction is causative of hyperexcitation, seizure spread and neurotoxicity. Accordingly, dysfunctional astrocytes should be considered as promising targets for new therapeutic strategies. In this review, we will summarize current knowledge of astrocyte dysfunction in temporal lobe epilepsy and discuss putative mechanisms underlying these alterations.