Abstract
Glucose-dependent periodic electrical activity of membranes of pancreatic islet cells1,2 mediates calcium uptake3,4, which is important for glucose-induced insulin release. As yet there has been no direct evidence identifying the ‘second messenger’ which couples the uptake and metabolism of glucose4 to the change of membrane electrical activity. Recent evidence showing that intracellular acidification stimulates islet B-cell electrical activity in a glucose-like manner has suggested that protons produced metabolically may serve as messengers by blocking K+ channels5 and depolarizing the membrane. Thus protons have been suggested6 to inhibit the Ca2+-activated K+-conductance [GK(Ca)] which is thought5–9 to produce the ‘pacemaker’ current responsible for the rhythmic firing of plateau depolarizations10 and Ca2+ spikes11. Although these conductance channels have been characterized at the single channel level in several tissues12–18, little is known of their response to intracellular pH (ref. 19) and they have not yet been characterized in B-cells. We have, therefore, used the patch-clamp method to study identified rat B-cells and show here that the B-cell GK(Ca) channel is activated by membrane depolarization as well as by cytoplasmic Ca2+, while it is inhibited by acidification of the cytoplasmic membrane surface.
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Cook, D., Ikeuchi, M. & Fujimoto, W. Lowering of pHi inhibits Ca2+-activated K+ channels in pancreatic B-cells. Nature 311, 269–271 (1984). https://doi.org/10.1038/311269a0
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DOI: https://doi.org/10.1038/311269a0
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