Astrocytes as new targets for antiepileptic drugs

Epilepsy is a disorder of the brain characterised by un-provoked, recurrent seizures and affects about 1% of the population worldwide. A deeper understanding of the cellular basis of the epilepsies would be essential for the identification of novel targets for therapeutic intervention. Since neuronal hyperexcitation and hypersynchronization are hallmarks of epilepsy, the search for new antiepileptic drugs (AEDs) has concentrated so far mainly on compounds that affect neuronal functions. However, the efficacy and tolerability of these drugs have not substantially improved over the past decades, and all known AEDs merely suppress the symptoms without treating the underlying disorder. Hence, new strategies for the development of more effica-cious AEDs are required. In this context glial cells, astrocytes in particular, have attracted increasing attention. These cells play essential roles in brain physiology: they modulate synaptic transmission by release, uptake, degradation and recycling of transmitters, and control ion homeostasis and blood–brain-barrier integrity. Impairment of these functions has been associated with the pathophysiology of epilepsy. This symposium will highlight an alternative view on the etiopathogenesis of epilepsy and challenge the commonly accepted neurocentric view of epileptogenesis. We will bring together scientists with basic research background and practising clinicians working on different aspects of neuron-glia interactions in epilepsy. The symposium will be opened by Peter Bedner with a brief introduction to clinical and neuropathological characteristics of epilepsy and the possible role of dysfunctional astrocytes in the development and progression of the disorder. The first speaker, Tore Eid, will talk about the astrocytic regulation of glutamate homeostasis in epilepsy. Eleonora Aronica will reveal the role of astrocyte immune responses in epilepsy. Kjell Heu-ser will present new evidence of altered astrocytic Ca 2+ signaling in the early stage of epileptogenesis. Finally, Peter Bedner will discuss the involvement of impaired astrocytic gap junction coupling in the development and progression of temporal lobe epilepsy.