Serum of Isaacs' syndrome suppresses potassium channels in PC-12 cell lines.
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.
Sonoda
Y
Y
Third Department of Internal Medicine, Kagoshima University School of Medicine, Japan.
Arimura
K
K
Kurono
A
A
Suehara
M
M
Kameyama
M
M
Minato
S
S
Hayashi
A
A
Osame
M
M
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D004553:Electric Conductivity; D005207:Fasciculation / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D016716:PC12 Cells / Q000378:metabolism; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D013997:Time Factors
D026902:Potassium Channel Blockers; D015221:Potassium Channels