Enhancement of beta-adrenergic receptor activation of maxi-K+ channels by GM1 ganglioside.
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.
Fan
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SF
Department of Physiology and Biophysics, State University of New York at Stony Brook, 11794.
Wang
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S
Kao
C Y
CY
D000818:Animals; D002772:Cholera Toxin / Q000494:pharmacology; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D006168:Guinea Pigs; D066298:In Vitro Techniques; D015640:Ion Channel Gating; D007545:Isoproterenol / Q000494:pharmacology; D009130:Muscle, Smooth; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
D015221:Potassium Channels; D011943:Receptors, Adrenergic, beta; D005677:G(M1) Ganglioside; D002772:Cholera Toxin; D007545:Isoproterenol; D011188:Potassium