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Serum of Isaacs' syndrome suppresses potassium channels in PC‐12 cell lines
Author(s) -
Sonoda Yoshito,
Arimura Kimiyoshi,
Kurono Asutsugu,
Suehara Masahito,
Kameyama Masaki,
Minato Seiichi,
Hayashi Akito,
Osame Mitsuhiro
Publication year - 1996
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880191102
Subject(s) - patch clamp , potassium channel , endocrinology , medicine , chemistry , cell culture , antibody , perfusion , potassium , clamp , electrophysiology , microbiology and biotechnology , immunology , biology , genetics , mechanical engineering , clamping , organic chemistry , engineering
Blockage of K + channels in nerve terminals by immunoglobulin is the speculated pathomechanism of Isaacs' syndrom. Using patch‐clamp technique (whole‐cell clamp), we investigated the effects on K + current of serum taken from 2 patients with Isaacs' syndrom employing the clonal cell line PC‐12. The addition of a patient's serum to the perfusion solution had little effect on the K + current of P‐12 cells. In contrast, K + current was reduced by 25–80% when cells were cultured for 3–6 days with 2% serum as compared to control serum values. Supperession of the K + current appears to develop gradually over the period of culture. Our results suggest that the pathomechanism of Isaacs' syndrome is caused by K + channel suppression via a humoral factor(s) in the serum, which subsequently induces nerve hyperexcitability. © 1996 John Wiley & Sons, Inc.
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