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

被引:59
作者
Yoshimoto, Y
Fukuyama, Y
Horio, Y
Inanobe, A
Gotoh, M
Kurachi, Y
机构
[1] Osaka Univ, Fac Med, Dept Pharmacol 2, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Med, Osaka 5650871, Japan
[3] Osaka Univ, Fac Pharmaceut Sci, Dept Pharmacol, Osaka 5650871, Japan
[4] Fukushima Med Univ, Dept Surg 1, Fukushima 9601295, Japan
基金
日本学术振兴会;
关键词
G protein-gated K+ channel; hyperpolarization; pancreatic alpha cell; somatostatin; patch clamp; immunohistochemistry;
D O I
10.1016/S0014-5793(99)00076-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Somatostatin inhibits glucagon-secretion from pancreatic alpha cells but its underlying mechanism is unknown. In mouse alpha 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), GTP gamma S or G beta gamma 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 alpha cells. (C) 1999 Federation of European Biochemical Societies.
引用
收藏
页码:265 / 269
页数:5
相关论文
共 29 条
[1]   DOES GALANIN INHIBIT INSULIN-SECRETION BY OPENING OF THE ATP-REGULATED K+ CHANNEL IN THE BETA-CELL [J].
AHREN, B ;
BERGGREN, PO ;
BOKVIST, K ;
RORSMAN, P .
PEPTIDES, 1989, 10 (02) :453-457
[2]   AN ENZYMATIC MECHANISM FOR POTASSIUM CHANNEL STIMULATION THROUGH PERTUSSIS-TOXIN-SENSITIVE G-PROTEINS [J].
ARMSTRONG, DL ;
WHITE, RE .
TRENDS IN NEUROSCIENCES, 1992, 15 (10) :403-408
[3]   CLONING AND FUNCTIONAL EXPRESSION OF THE CDNA-ENCODING AN INWARDLY-RECTIFYING POTASSIUM CHANNEL EXPRESSED IN PANCREATIC BETA-CELLS AND IN THE BRAIN [J].
BOND, CT ;
AMMALA, C ;
ASHFIELD, R ;
BLAIR, TA ;
GRIBBLE, F ;
KHAN, RN ;
LEE, K ;
PROKS, P ;
ROWE, ICM ;
SAKURA, H ;
ASHFORD, MJ ;
ADELMAN, JP ;
ASHCROFT, FM .
FEBS LETTERS, 1995, 367 (01) :61-66
[4]   ATRIAL G-PROTEIN-ACTIVATED K+-CHANNEL - EXPRESSION CLONING AND MOLECULAR-PROPERTIES [J].
DASCAL, N ;
SCHREIBMAYER, W ;
LIM, NF ;
WANG, WZ ;
CHAVKIN, C ;
DIMAGNO, L ;
LABARCA, C ;
KIEFFER, BL ;
GAVERIAUXRUFF, C ;
TROLLINGER, D ;
LESTER, HA ;
DAVIDSON, N .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (21) :10235-10239
[5]  
DEWEILLE J, 1988, P NATL ACAD SCI USA, V85, P1312
[6]  
DEWEILLE JR, 1989, P NATL ACAD SCI USA, V86, P2971
[7]  
DOLPHIN AC, 1989, ANN NY ACAD SCI, V560, P387, DOI 10.1111/j.1749-6632.1989.tb24117.x
[8]   GALANIN AND EPINEPHRINE ACT ON DISTINCT RECEPTORS TO INHIBIT INSULIN RELEASE BY THE SAME MECHANISMS INCLUDING AN INCREASE IN K+ PERMEABILITY OF THE B-CELL MEMBRANE [J].
DREWS, G ;
DEBUYSER, A ;
NENQUIN, M ;
HENQUIN, JC .
ENDOCRINOLOGY, 1990, 126 (03) :1646-1653
[9]   HETEROLOGOUS MULTIMERIC ASSEMBLY IS ESSENTIAL FOR K+ CHANNEL ACTIVITY OF NEURONAL AND CARDIAC G-PROTEIN-ACTIVATED INWARD RECTIFIERS [J].
DUPRAT, F ;
LESAGE, F ;
GUILLEMARE, E ;
FINK, M ;
HUGNOT, JP ;
BIGAY, J ;
LAZDUNSKI, M ;
ROMEY, G ;
BARHANIN, J .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 212 (02) :657-663
[10]   PANCREATIC-ISLET CELLS EXPRESS A FAMILY OF INWARDLY RECTIFYING K+ CHANNEL SUBUNITS WHICH INTERACT TO FORM G-PROTEIN-ACTIVATED CHANNELS [J].
FERRER, J ;
NICHOLS, CG ;
MAKHINA, EN ;
SALKOFF, L ;
BERNSTEIN, J ;
GERHARD, D ;
WASSON, J ;
RAMANADHAM, S ;
PERMUTT, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (44) :26086-26091