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Serum of Isaacs' syndrome suppresses potassium channels in PC-12 cell lines
Y Sonoda1, K Arimura, A Kurono
1Third Department of Internal Medicine, Kagoshima University School of Medicine, Japan.
Blockage of K+ channels in nerve terminals by immunoglobulin is the speculated pathomechanism of Isaacs' syndrome. Using patch-clamp technique (whole-cell clamp), we investigated the effects on K+ current of serum taken from 2 patients with Isaacs' syndrome 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. Suppression 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.
Blockage of K+ channels in nerve terminals by immunoglobulin is the speculated pathomechanism of Isaacs' syndrome. Using patch-clamp technique (whole-cell clamp), we investigated the effects on K+ current of serum taken from 2 patients with Isaacs' syndrome 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. Suppression 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.