Tetraethylammonium modifies gap junctions between pancreatic beta-cells.
Gap junctions between pancreatic beta-cells were quantitatively assessed in freeze-fracture replicas of isolated rat islets of Langerhans incubated for 90 min with or without the potassium conductance blocker tetraethylammonium (TEA). The results show that TEA increases the median number of particles per beta-cell gap junction but not the frequency of gap junctions at both nonstimulating and threshold-stimulating concentrations of glucose. TEA increased the relative gap junctional area at both concentrations of glucose. TEA had no effect on insulin release at a basal concentration of glucose but potentiated that release at the threshold glucose level. Thus TEA modifies beta-cell gap junctions independently of its effect on insulin release. However, the junctional changes observed were greater when insulin release was also elevated.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002478:Cells, Cultured; D005614:Freeze Fracturing; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007365:Intercellular Junctions / Q000648:ultrastructure*; D007515:Islets of Langerhans / Q000378:metabolism / Q000648:ultrastructure*; D008297:Male; D008854:Microscopy, Electron; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*
D007328:Insulin; D013757:Tetraethylammonium Compounds; D012964:Sodium; D011188:Potassium