Muscarinic receptor modulation of glucose‐induced electrical activity in mouse pancreatic B‐cells
Muscarinic receptor modulation of glucose‐induced electrical activity in mouse pancreatic B‐cells
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小鼠胰腺 B 细胞中葡萄糖诱导的电活动的毒蕈碱受体调节
DOI：
10.1016/0014-5793(89)80669-6
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发表时间：
1989
期刊：
影响因子：
3.5
通讯作者：
E. Rojas
中科院分区：
文献类型：
--
作者：
R. M. Santos;E. Rojas
乙酰胆碱(1-10μM)使小鼠胰腺B细胞膜去极化，并刺激葡萄糖引起的电活动爆发。乙酰胆碱的作用与毒扁豆碱相似，而尼古丁对膜电位无影响。经典M1型受体拮抗剂哌仑西平可拮抗乙酰胆碱对葡萄糖诱发的电活动，而M2受体拮抗剂加拉胺(1-100μM)则不能拮抗乙酰胆碱对葡萄糖诱发的电活动的作用(IC_(50)=0.25μM)。Bethanecol是经典的M2-型M受体的激动剂，在刺激电活动方面的效果大约是乙酰胆碱的100倍。此外，乙酰胆碱(1μM)引起B细胞膜输入阻力显著增加(25%)。结果表明，乙酰胆碱通过激活一种不同于经典M2型受体的M受体亚型来抑制K+传导，从而对B细胞膜起作用。
Acetylcholine (1–10 μM) depolarized the membrane and stimulated glucose-induced bursts of electrical activity in mouse pancreatic B-cells. The acetylcholine effects were mimicked by muscarine while nicotine had no effect on membrane potential. Pirenzepine, an antagonist of the classical M1-type muscarinic receptors, but not gallamine (1–100 μM), an antagonist of the classical M2-type receptors, antagonized the acetylcholine action on glucose-induced electrical activity (IC50= 0.25 μM). Bethanechol, an agonist of the classical M2-type muscarinic receptors, was approximately 100 times less effective than acetylcholine in stimulating the electrical activity. In addition, acetylcholine (1 μM) induced a marked increase (25%) in input resistance to the B-cell membrane. The results indicate that acetylcholine exerted its effects on the B-cell membrane by inhibiting K+conductance via activation of a muscarinic receptor subtype distinct from the classical M2-type receptor.
神经元毒蕈碱受体与反应的耦合。
DOI：
10.1146/annurev.pa.24.040184.001005
发表时间：
1984
影响因子：
12.5
作者：
McKinney,M;Richelson,E
通讯作者：
Richelson,E
胆碱能激动剂抑制蟾蜍新鲜分离的平滑肌细胞中的钾电流。
DOI：
10.1113/jphysiol.1985.sp015837
发表时间：
1985
期刊：
The Journal of physiology
影响因子：
--
作者：
Sims,SM;Singer,JJ;WalshJr,JV
通讯作者：
WalshJr,JV