The electrical responsiveness of pancreatic β-cells can be temporally potentiated after the exposure to certain agents. An interesting case, due to its potential physiological relevance, is the temporal potentiation of sensitivity (TPS) to glucose after exposure to carbachol that we have previously described. Due to its temporal nature, a molecule activation after glucose and carbachol exposure can be supposed to be present once the stimulus has disappeared. To elucidate whether this molecule is present before carbachol application or has to be produced by the muscarinic stimulation (de novo synthesis) we have applied our stimulation protocol in the presence of an inhibitor of protein synthesis, cycloheximide. The islets of Langerhans were previously incubated for 2 h with the protein inhibitor. We found that with inhibition of protein synthesis, TPS remains unchanged. The quantitative analysis shows a mean increase of 70% in the first pulse after carbachol application, a mean increase of 60% in the second pulse and a mean increase of 30% in the third pulse; these increases are not significantly different from that obtained with control stimulation. These results show the independence of TPS on de novo protein synthesis.

This study was financed by SAF2001-3401-C02-01.