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蛋白偶联受体\u002FG 蛋白\n>>\n5-HT受体\n信号通路\n>>\n神经信号通路\n>>\n5-HT受体\n信号通路\n>>\nG 蛋白偶联受体\u002FG 蛋白\n>>\n肾上腺素能受体\n信号通路\n>>\nG 蛋白偶联受体\u002FG 蛋白\n>>\n多巴胺受体\n信号通路\n>>\n神经信号通路\n>>\n多巴胺受体\n研究领域\n>>\n神经疾病",{"key":234,"value":235},"靶点","Ki: 0.71 nM (dopamine D3 receptor), 4-15 nM (dopamine D2, D5, D4 receptors), 83 nM (dopamine D1 receptor)[1][2], 176 nM (α1A), 273 nM (α1B), 338 nM (α2A), 27 nM (α2B), 30 nM (5-HT1A), 86 nM (5-HT7)[2]",{"key":237,"value":238},"体外研究","与D2,D4和D5(pKi 8.5-8.0)相比,Rotigotine对D3(pKi9.2)受体具有10倍的选择性,与D1受体(pKi7.2)相比具有100倍的选择性。在功能研究中,罗替戈汀在所有多巴胺受体中表现为完全激动剂,但值得注意的是,D1受体刺激的效力与D2和D3受体相似(分别为pEC50：9.0,9.4-8.6,9.7)[1]。在原代中脑细胞培养中,罗替戈汀(10μM)使THir神经元的数量减少40％。 Rotigotine(0.01μM)略微保护多巴胺能神经元免受MPP +毒性,显着保护多巴胺能神经元免受鱼藤酮诱导的细胞死亡,并显着抑制鱼藤酮产生ROS [4]。",{"key":240,"value":241},"体内研究","在引发的大鼠中,罗替戈汀(0.035,0.1和0.35mg\u002Fkg)以剂量依赖性方式诱导对侧转向行为。在药物天然大鼠中,与引发的大鼠相比,单独或与SCH 39166组合的罗替戈汀诱导的转向行为减少[3]。",{"key":243,"value":244},"激酶实验","结合测定在96孔聚丙烯管中进行，D1和D4膜的最终体积为2mL，D2，D3和D5膜的1mL，含有：50μL放射性配体，10μL药物\u002F缓冲液\u002F非特异性结合，缓冲液（终浓度50mM Tris-HCl pH 7.4，MgCl 2 2mM）和膜（D2和D3为5μg蛋白质，D1和D5为25μg蛋白质）。在25℃温育120分钟后，通过预浸在0.1％聚乙烯亚胺中的A \u002F C玻璃纤维滤器快速真空过滤测定结合的放射性配体。将滤器用2mL冰冷的灰化缓冲液（Tris-HCl 50mM，pH 7.4,4℃）洗涤四次，并通过液体闪烁计数测定保留的放射性。",{"key":246,"value":247},"动物实验","引发的大鼠：在6-OHDA损伤后两周，用阿扑吗啡（0.5mg \u002F kg sc）引发大鼠。在1小时测试期间显示少于150个对侧旋转的大鼠被排除在研究之外。引发后3天，将大鼠分成不同的实验组，并用不同剂量的多巴胺受体激动剂（罗替戈汀或普拉克索）单独或与多巴胺D1（SCH 39166）或D2（依替必利）受体拮抗剂联合治疗，如报道：生理盐水+罗替戈汀（0.035mg \u002F kg sc，n = 9; 0.1mg \u002F kg sc，n = 9; 0.35mg \u002F kg sc，n = 8）; SCH 39166（0.1mg \u002F kg sc）+罗替戈汀（0.035mg \u002F kg sc，n = 5; 0.1mg \u002F kg sc，n = 7; 0.35mg \u002F kg sc，n = 5）;依替洛普（0.1mg \u002F kg sc）+罗替戈汀（0.1mg \u002F kg sc，n = 5; 0.35mg \u002F kg sc，n = 5）;盐水+普拉克索（0.035mg \u002F kg sc，n = 5; 0.1mg \u002F kg sc，n = 12; 0.35mg \u002F kg sc，n = 7）; SCH 39166（0.1mg \u002F kg sc）+普拉克索（0.035mg \u002F kg sc，n = 5; 0.1mg \u002F kg sc，n = 6; 0.35mg \u002F kg sc，n = 6）;依替必利（0.1mg \u002F kg sc）+普拉克索（0.1mg \u002F kg sc，n = 7; 0.35mg \u002F kg sc，n = 5）。",{"key":249,"value":250},"参考文献","[1].\nWood M, et al. Rotigotine is a potent agonist at dopamine D1 receptors as well as at dopamine D2 and D3 receptors. Br J Pharmacol. 2015 Feb;172(4):1124-35.\n[2].\nScheller D, et al. The in vitro receptor profile of rotigotine: a new agent for the treatment of Parkinson's disease. Naunyn Schmiedebergs Arch Pharmacol. 2009 Jan;379(1):73-86.\n[3].\nFenu S, et al. In vivo dopamine agonist properties of rotigotine: Role of D1 and D2 receptors. Eur J Pharmacol. 2016 Oct 5;788:183-91.\n[4].\nRadad K, et al. Neuroprotective effect of rotigotine against complex I inhibitors, MPP? and rotenone, in primary mesencephalic cell culture. 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