A Novel ATP-dependent Inward Rectifier Potassium Channel Expressed Predominantly in Glial Cells

doi:10.1074/jbc.270.27.16339

A Novel ATP-dependent Inward Rectifier Potassium Channel Expressed Predominantly in Glial Cells (*)

From the (1)Department of Pharmacology II, Department of Obstetrics and Gynecology,
(2)Department of Neuroanatomy, Biomedical Research Center, Faculty of Medicine Osaka University, Suita, Osaka 565, Japan and
(3)Institute for Immunology, Kyoto University Faculty of Medicine, Sakyo, Kyoto 606-01, Japan

^§ To whom correspondence should be addressed:
Dept. of Pharmacology II, Faculty of Medicine Osaka University, Yamada-oka 2-2, Suita, Osaka 565, Japan.
Tel.: 81-6-879-3510; Fax: 81-6-879-3519.

Abstract

We have isolated a novel inward rectifier K channel predominantly expressed in glial cells of the central nervous system. Its amino acid sequence exhibited 53% identity with ROMK1 and approximately 40% identity with other inward rectifier K channels. Xenopus oocytes injected with cRNA derived from this clone expressed a K current, which showed classical in-ward rectifier K channel characteristics. Intracellular MgATP was required to sustain channel activity in excised membrane patches, which is consistent with a Walker type-A ATP-binding domain on this clone. We designate this new clone as K-2 (the second type of inward rectifying K channel with an ATP-binding domain). In situ hybridization showed K-2 mRNA to be expressed predominantly in glial cells of the cerebellum and forebrain. This is the first description of the cloning of a glial cell inward rectifier potassium channel, which may be responsible for K buffering action of glial cells in the brain.

Footnotes

↵* This work was supported in part by research grants from the Ministry of Education, Science, and Culture of Japan, the Terumo Life Science Foundation, the Ichiro Kanehara Foundation, the Yamanouchi Foundation for Research on Metabolic Disorders, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, the Naito Foundation, Ono Pharmaceutical Company (to Y. K.), and the Kanae Foundation of Research for New Medicine (to T. T.). The contributions of the first two authors should be considered as equal. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore by hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank/EMBL Data Bank with accession number(s) X86818.
↵¹ The abbreviations used are:

E^K

equilibrium potential for K

ROMK

inwardly rectifying ATP-regulated potassium channel from the outer medulla of rat kidney

IRK

inward rectifier potassium channel

GIRK

G protein-activated muscarinic potassium channel

K

ATP-sensitive potassium channel

K

inward rectifying K channel with an ATP-binding domain

PCR

polymerase chain reaction

[K]

external potassium ion concentration

S

siemen(s)

P^o

open probability

time constant.
↵² K. Morishige, N. Takahashi, M. Yamada, N. Mori, and Y. Kurachi, unpublished data.
↵³ Y. Horio, A. Inanobe, T. Takumi, and Y. Kurachi, unpublished data.