Department of Pharmacology, Sapporo Medical School, School of Medicine, South 1, West 17, Chu-ouku, Sapporo 060-8556, Japan
*Corresponding author. FAX: +81-11-612-5861, E-mail: email@example.com
Abstract: Firing of neurons changes the extracellular concentration of K+ ions ([K+]o). Glial cells have the ability to maintain [K+]o at a constant level. This function has been called "K+-spatial buffering". K+ channels are believed to be involved in K+-spatial buffering. Kir4.1 in retinal glial cells and Kir2.1, Kir2.3 and Kv1.5 in Schwann cells have been identified. All of these K+ channels show polarized distribution, which enables the channels to transport K+ ions to appropriate regions such as blood vessels and the vitreous body. These channels have a consensus C-terminal sequence that can bind a protein containing PDZ (PSD-95/dlg/ZO1) domains, which may regulate the distribution of the channels. Kir4.1 is predominantly expressed in membranes adjacent to basement membranes. Laminin, a component of basement membranes, is necessary for the surface expression of Kir4.1 in cultured retinal glial cells, suggesting that an extracellular signal regulates the function of glial cells. In some cases, K+ buffering has been considered to couple tightly with water flux. Actually the aquaporin-4 water channel has been found to colocalize with Kir4.1 in retinal glial cells. Recent studies of K+ channels have elucidated the mechanisms of old well-known phenomena and present new unknown roles of glial cells.
Keywords: K+ channel, Glia, Water channel, PDZ domain, Laminin
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