Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

Pflugers Arch

Publication Date

04/2001

Volume

442

Pages

19 - 26

Keywords

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