Astrocytes sense and respond to synaptic activity through activation of different neurotransmitter receptors and transporters. Astrocytes are also coupled by gap junctions, which allow these cells to redistribute through the glial network the K⁺ ions excessively accumulated at sites of intense neuronal activity. Work over the past two decades has revealed important roles for astrocytes in brain physiology, and it is therefore not surprising that recent studies unveiled their involvement in the etiology of neurological disorders such as epilepsy. Investigation of specimens from patients with pharmacoresistant temporal lobe epilepsy and epilepsy models revealed alterations in expression, localization and function of astrocytic connexins, K⁺ and water channels. In addition, disturbed gliotransmission as well as malfunction of glutamate transporters and of the astrocytic glutamate- and adenosine-converting enzymes – glutamine synthetase and adenosine kinase, respectively – have been observed in epileptic tissues. Accordingly, increasing evidence indicates that dysfunctional astrocytes are crucially involved in processes leading to epilepsy. These new insights might foster the search for new targets for the development of new, more efficient anti-epileptogenic therapies.