Fan S F, Wang S, Kao C Y
Department of Physiology and Biophysics, State University of New York at Stony Brook, 11794.
Biochem Biophys Res Commun. 1994 May 16;200(3):1341-5. doi: 10.1006/bbrc.1994.1598.
In freshly dispersed guinea-pig taenia coli myocytes, beta-adrenergic receptor agonist isoproterenol (ISO, 2-5 microM) increased the open probability (po) of the maxi-K+ channels through the G-protein, G. Subunit B of cholera toxin (0.1 nM) suppressed the ISO-induced increase of po of maxi-Ks+ channels but did not affect that induced by forskolin. Brief (20 min) treatment of the myocytes with GM1 ganglioside (GM1, 0.1-1.0 microM) enhanced the effectiveness of ISO-induced increase of po. This effect was blocked by 0.5% trypsin, which is known to prevent the incorporation of exogeneous GM1 into the membrane. The effect of GM1 was not shared by GM2 and GM3 gangliosides. These results suggest that the membrane-bound endogeneous GM1 may participate in the regulation of cellular response to beta-adrenergic agents.
在新鲜分离的豚鼠结肠带肌细胞中，β-肾上腺素能受体激动剂异丙肾上腺素（ISO，2 - 5微摩尔）通过G蛋白增加大电导钾通道的开放概率（po）。霍乱毒素的G亚基B（0.1纳摩尔）抑制了ISO诱导的大电导钾通道po增加，但不影响福斯可林诱导的增加。用GM1神经节苷脂（GM1，0.1 - 1.0微摩尔）对肌细胞进行短暂（20分钟）处理可增强ISO诱导的po增加的效果。这种作用被0.5%的胰蛋白酶阻断，已知胰蛋白酶可阻止外源性GM1掺入膜中。GM2和GM3神经节苷脂没有GM1的这种作用。这些结果表明，膜结合的内源性GM1可能参与细胞对β-肾上腺素能药物反应的调节。
