Somatostatin induces hyperpolarization in pancreatic islet α cells by activating a G protein‐gated K+ channel

FEBS Letters

Gotoh, Mitsukazu¹  Horio, Yoshiyuki²  Fukuyama, Yuji²  Inanobe, Atsushi²  Kurachi, Yoshihisa²  Yoshimoto, Yukiko² 

[1]Department of Surgery I, Fukushima Medical University, 1 Hikarigaoka, Fukushima, Fukushima 960-1295, Japan

[2]Department of Pharmacology II, Faculty of Medicine and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan

关键词: G protein-gated K+ channel;    Hyperpolarization;    Pancreatic α cell;    Somatostatin;    Patch clamp;    Immunohistochemistry;   

DOI  :  10.1016/S0014-5793(99)00076-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Somatostatin inhibits glucagon-secretion from pancreatic α cells but its underlying mechanism is unknown. In mouse α cells, we found that somatostatin induced prominent hyperpolarization by activating a K⁺ channel, which was unaffected by tolbutamide but prevented by pre-treating the cells with pertussis toxin. The K⁺ channel was activated by intracellular GTP (with somatostatin), GTPγS or Gβγ subunits. It was thus identified as a G protein-gated K⁺ (K_G) channel. RT-PCR and immunohistochemical analyses suggested the K_G channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin-inhibition of glucagon-secretion from pancreatic α cells.

【 授权许可】

Unknown