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Somatostatin hyperpolarized rat pancreatic alpha-cells and inhibited spontaneous electrical activity by activating a low-conductance K+ channel (0.9 pS with physiological ionic gradients). This channel was insensitive to tolbutamide (a blocker of ATP-sensitive K+ channels) and apamin (an inhibitor of small-conductance Ca(2+)-activated K+ channels). Channel activation was prevented by pre-treating the cells with pertussis toxin, indicating the involvement of G-proteins. A direct interaction between an inhibitory G-protein and the somatostatin-activated K+ channel is suggested by the finding that intracellular application of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma-S) and the G beta gamma subunit of G-proteins resulted in a transient stimulation of the current. Activation of the K+ current by somatostatin was inhibited by intracellular dialysis with specific antibodies to Gi1/2 and was not seen in cells treated with antisense oligonucleotides against G-proteins of the subtype Gi2. We conclude that somatostatin suppresses alpha-cell electrical activity by a Gi2-protein-dependent mechanism, which culminates in the activation of a sulphonylurea- and apamin-insensitive low-conductance K+ channel.


Journal article


Pflugers Arch

Publication Date





19 - 26


Animals, Antibodies, Apamin, Calcium, Dialysis, Electric Conductivity, GTP-Binding Protein alpha Subunits, Gi-Go, Guanosine 5'-O-(3-Thiotriphosphate), Islets of Langerhans, Male, Pertussis Toxin, Potassium Channel Blockers, Potassium Channels, Rats, Rats, Inbred Lew, Receptors, Somatostatin, Somatostatin, Tolbutamide, Virulence Factors, Bordetella