Yoshiyuki Horio*
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: horio@sapmed.ac.jp
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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