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Inward‐rectifying anion channels are expressed in the epithelial cells of choroid plexus isolated from ClC‐2 ‘knock‐out’ mice
Author(s) -
Speake Tracey,
Kajita Hidetoshi,
Smith Craig P.,
Brown Peter D.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2001.014548
Subject(s) - choroid plexus , microbiology and biotechnology , biology , cerebrospinal fluid , anatomy , membrane potential , chemistry , endocrinology , biophysics , neuroscience , central nervous system
Choroid plexus epithelial cells express inward‐rectifying anion channels which have a high HCO 3 − permeability. These channels are thought to have an important role in the secretion of cerebrospinal fluid. The possible relationship between these channels and the ClC‐2 Cl − channel was investigated in the present study. RT‐PCR, using specific ClC‐2 primers, amplified a 238 bp fragment of mRNA from rat choroid plexus, which was 99 % identical to the 5′ sequence of rat ClC‐2. A 2005 bp clone was isolated from a rat choroid plexus cDNA library using a probe for ClC‐2. The clone showed greater than 99 % identity with the sequence of rat ClC‐2. Inward‐rectifying anion channels were observed in whole‐cell recordings of choroid plexus epithelial cells isolated from ClC‐2 knock‐out mice. The mean inward conductance was 19.6 ± 3.6 nS ( n = 8 ) in controls (3 heterozygote animals), and 22.5 ± 3.1 nS ( n = 10 ) in three knock‐out animals. The relative permeability of the conductances to I − and Cl − ( P I : P Cl ) was determined. I − was more permeant than Cl − in both heterozygotes ( P I : P Cl = 4.0 ± 0.9, n = 3) and knock‐out animals ( P I : P Cl = 4.1 ± 1.4, n = 3). These results indicate that rat choroid plexus expresses the ClC‐2 variant that was originally reported in other tissues. ClC‐2 does not contribute significantly to inward‐rectifying anion conductance in mouse choroid plexus, which must therefore express a novel inward‐rectifying anion channel.