| Abstrakt: |
In mouse B-cells glucose induces a typical electrical activity consisting of slow waves of the membrane potential with spikes superimposed on the plateau. As the concentration of glucose is raised the number of spikes per minute increases. However, this increase could simply be due to the concomitant lengthening of the slow waves. We thus investigated whether glucose can influence spike activity when no slow waves occur. Persistent depolarization to the plateau potential was achieved at 3 mM glucose by tolbutamide or at 10 mM glucose by low Ca2+, by arginine or by ouabain. Under all these conditions, raising the concentration of glucose increased the spike frequency without changing the plateau potential. Similar effects were produced by tolbutamide which does not affect B-cell metabolism but directly blocks K+-ATP channels. The spike frequency could also be increased by arginine, which, however, consistently depolarized the membrane. In conclusion, spike activity in B-cells can be influenced by glucose independently from changes in slow wave duration. This indicates that some K+-ATP channels, a target for both glucose and tolbutamide, are still open when the membrane is depolarized at the plateau, or that these two agents share another yet unidentified target involved in spike generation. |
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