Structure and Function of Potassium Channels in Glia

A major effort in our laboratory aims to elucidate the role of inwardly rectifying potassium channels for glial cell function. Glial buffering of the extracellular potassium concentration in retina has been elegantly demonstrated using electrophysiological methods. Inwardly rectifying potassium channels in these glial cells are spatially localized to optimally perform this function. Research in our laboratory has established the essential role of Kir4.1 channel in mouse retina for the buffering of extracellular potassium concentration. More recently we have been investigating the role of accessory proteins for the modulation and subcellular localization of Kir4.1 channels in Müller cells. We have identified a potential macromolecular complex (Aquaporin-4, Kir4.1 and alpha syntrophin) that hold this cluster together. We are now expanding our research to glial cells in the brain and peripheral nervous system. Standing questions are: 1) Are Kir4.1 channels crucial for extracellular potassium buffering in the central and peripheral nervous system?, 2) Why mutations in Kir4.1 channel lead to neurological symptoms such as epilepsy, hearing loss and ataxia?; 3) What are the cellular mechanisms that control Kir4.1 channel density and expression in glial cells?