de Weille J, Schmid-Antomarchi H, Fosset M, Lazdunski M
Centre de Biochimie du Centre National de la Recherche Scientifique, Nice, France.
Proc Natl Acad Sci U S A. 1988 Feb;85(4):1312-6. doi: 10.1073/pnas.85.4.1312.
The action of the hyperglycemia-inducing hormone galanin, a 29-amino acid peptide named from its N-terminal glycine and C-terminal amidated alanine, was studied in rat insulinoma (RINm5F) cells using electrophysiological and 86Rb+ flux techniques. Galanin hyperpolarizes and reduces spontaneous electrical activity by activating a population of ATP-sensitive K+ channels with a single-channel conductance of 30 pS (at -60 mV). Galanin-induced hyperpolarization and reduction of spike activity are reversed by the hypoglycemia-inducing sulfonylurea glibenclamide. Glibenclamide blocks the galanin-activated ATP-sensitive K+ channel. 86Rb+ efflux from insulinoma cells is stimulated by galanin in a dose-dependent manner. The half-maximum value of activation is found at 1.6 nM. Galanin-induced 86Rb+ efflux is abolished by glibenclamide. The half-maximum value of inhibition is found at 0.3 nM, which is close to the half-maximum value of inhibition of the ATP-dependent K+ channel reported earlier. 86Rb+ efflux studies confirm the electrophysiological demonstration that galanin activates an ATP-dependent K+ channel.
利用电生理学和⁸⁶Rb⁺通量技术，在大鼠胰岛素瘤（RINm5F）细胞中研究了高血糖诱导激素甘丙肽（一种由其N端甘氨酸和C端酰胺化丙氨酸命名的29个氨基酸的肽）的作用。甘丙肽通过激活一群单通道电导为30 pS（在-60 mV时）的ATP敏感性钾通道，使细胞超极化并降低自发电活动。甘丙肽诱导的超极化和动作电位活动的降低可被低血糖诱导剂磺酰脲类药物格列本脲逆转。格列本脲可阻断甘丙肽激活的ATP敏感性钾通道。甘丙肽以剂量依赖性方式刺激胰岛素瘤细胞中的⁸⁶Rb⁺外流。激活的半数最大值在1.6 nM处发现。甘丙肽诱导的⁸⁶Rb⁺外流被格列本脲消除。抑制的半数最大值在0.3 nM处发现，这接近于先前报道的ATP依赖性钾通道抑制的半数最大值。⁸⁶Rb⁺外流研究证实了电生理学证明，即甘丙肽激活了一个ATP依赖性钾通道。
