Characterization of muscarinic receptor-mediated cationic currents in longitudinal smooth muscle cells of mouse small intestine
Characterization of muscarinic receptor-mediated cationic currents in longitudinal smooth muscle cells of mouse small intestine
复制标题
DOI：
10.1254/jphs.fp0050973
复制
发表时间：
2006-03-01
影响因子：
3.5
通讯作者：
Komori, S
中科院分区：
文献类型：
--
作者：
Sakamoto, T;Unno, T;Komori, S
在保持在-50 mV的小鼠小肠平滑肌细胞上，卡巴胆碱在细胞内Cs+存在的情况下诱发阿托品敏感的内向电流。电流响应由一个初始峰值和一个较小的平台分量组成，在该平台上经常出现振荡电流。不同实验过程的结果表明，内向电流是一种M受体控制的阳离子电流，对细胞内钙离子浓度([Ca~(2+)](I))敏感，起始峰和振荡成分被钙激活的氯离子电流污染。在[Ca~(2+)]i缓冲至100W的条件下，对卡巴胆碱累积施药的MI(CAT)反应被W选择性拮抗剂竞争性抑制，而被M-3选择性拮抗剂非竞争性抑制。此外，百日咳毒素(PTX)处理或磷脂酶C(PLC)抑制剂也可使其严重减少。对小鼠和豚鼠肠肌细胞MI(CAT)的比较分析表明，这两种细胞的潜在通道在激动剂敏感性、电流-电压关系和单位电导方面相似。结果表明，在小鼠肠肌细胞中，m1(CAT)主要通过一种M-2/M-3协同机制产生，该机制涉及PTX敏感的G蛋白和PLC活性，而不受[Ca~(2+)]i变化的电流调制，如豚鼠回肠心肌(CAT)。在这两种类型的心肌细胞之间，nil、下的通道在选通特性上也是难以区分的。
In mouse intestinal smooth muscle cells held at -50 mV, carbachol evoked an atropine-sensitive inward Current in the intracellular presence of Cs+. The current response consisted of an initial peak followed by a smaller plateau component on which oscillatory Currents frequently arose. Results from various experimental procedures indicated that the inward Current is a muscarinic receptor-operated cationic current sensitive to cytosolic Ca2+ concentration ([Ca2+](i)) and that the initial peak and oscillatory components are contaminated by Ca2+-activated Cl- currents. Under conditions of [Ca2+] i buffered to 100 W, the mI(cat) response to cumulative carbachol applications was inhibited competitively by an W-selective antagonist but non-competitively by an M-3-selective one. Also it was severely reduced by pertussis toxin (PTX) treatment or a phospholipase C (PLC) inhibitor. Comparative analysis of mI(cat) in mouse and guinea-pig intestinal myocytcs indicated that the underlying channels resemble between those myocytes in agonist sensitivity, current-voltage relationship, and unitary conductance. The results Suggest that in mouse intestinal myocytes, ml(cat) arises mainly via an M-2/M-3 synergistic mechanism involving PTX-sensitive G-proteins and PLC activity in the absence of current modulation by [Ca2+]i changes, as described for guinea-pig ileal mI(cat). The channels underlying nil,,,, are also indistinguishable in gating properties between both types of myocytes.