RESEARCH

Our laboratory has long been interested on the mechanisms by which neurotransmitters modulate the excitability of neuronal and glial cells. Molecular effectors for such modulation are for example potassium channels, a large and diverse class of transmembrane proteins that mediate the controlled flux of potassium ions. Currently we are working with the G protein-gated inwardly rectifying potassium (GIRK) channels. GIRK channels open upon activation of metabotropic receptors (e.g.opioids, muscarinic, adrenergic receptors) that couple to the Gi or Go class of G proteins. We are employing the heterologous expression of GIRK channels and various metabotropic receptors to investigate how this signaling takes place.

Another major effort in our laboratory aims to elucidate the role of inwardly rectifying potassium channels in 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.