Inhibitory effects of anesthetics and ethanol on muscarinic receptors expressed in Xenopus oocytes.
Inhibitory effects of anesthetics and ethanol on muscarinic receptors expressed in Xenopus oocytes.
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麻醉剂和乙醇对非洲爪蟾卵母细胞表达的毒蕈碱受体的抑制作用。
DOI：
10.1016/s0014-2999(97)01354-x
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发表时间：
1997
影响因子：
5
通讯作者：
Harris,RA
中科院分区：
文献类型：
--
作者：
Minami,K;Vanderah,TW;Minami,M;Harris,RA
众所周知，麻醉剂（和乙醇）会产生健忘症和固定。最近鉴定的非固定（非麻醉）剂（F6或1，2-二氯六氟环丁烷），损害学习和记忆表明，不同的机制可能是负责这两个行动的麻醉剂。毒蕈碱受体被认为在记忆和学习中起作用，我们询问这些受体的特定亚型是否受到麻醉剂和新的非麻醉剂的影响。我们研究了氟烷，一种新的卤代麻醉剂化合物F3（1-氯-1，2，2-三氟环丁烷）和乙醇对乙酰胆碱诱导电流的影响，乙酰胆碱诱导电流由非洲爪蟾卵母细胞中表达的毒蕈碱m1受体介导。我们还研究了卤代非麻醉化合物F6和F8（2，3-氯八氟丁烷）对M_1受体的影响。氟烷、F3、F6和乙醇在浓度相关时抑制毒蕈碱m1受体诱导的Ca 2+依赖性Cl−电流。F8对乙酰胆碱诱导的毒蕈碱m1受体功能无影响。蛋白激酶C抑制剂双吲哚马来酰亚胺I（GF 109203 X）增强乙酰胆碱诱导的电流，蛋白激酶C激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）抑制该电流。GF 109203 X可阻断氟烷、F3和乙醇对M_1受体的抑制作用，但对F6的作用无影响。这些结果表明，麻醉剂和非麻醉剂抑制毒蕈碱m1受体的功能，并建议激活蛋白激酶C作为麻醉剂和乙醇对这些受体的作用机制。
Anesthetics (and ethanol) are known to produce amnesia as well as immobilization. Recent identification of a nonimmobilizing (nonanesthetic) agent (F6 or 1,2-dichlorohexafluorocyclobutane) that impairs learning and memory suggests that distinct mechanisms may be responsible for these two actions of anesthetic agents. Muscarinic receptors are believed to play a role in memory and learning, and we asked if a specific subtype of these receptors is affected by anesthetics as well as the new nonanesthetic. We investigated the effects of halothane, a novel halogenated anesthetic compound F3 (1-chloro-1,2,2-trifluorocyclobutane) and ethanol on acetylcholine-induced current mediated by a muscarinic m1receptor expressed in Xenopus oocytes. We also studied the effects of halogenated nonanesthetic compounds, F6 and F8 (2,3-chlorooctafluorobutane) on muscarinic m1receptors. Halothane, F3, F6 and ethanol inhibited muscarinic m1receptor-induced Ca2+-dependent Cl−currents at pharmacologically relevant concentrations. F8 had no effect on acetylcholine-induced muscarinic m1receptor function. The protein kinase C inhibitor, bisindolylmaleimide I (GF109203X), enhanced the acetylcholine-induced current and the protein kinase C activator, phorbol 12-myristate 13-acetate (PMA), inhibited this current. GF109203X abolished the inhibitory effects of halothane, F3 and ethanol on muscarinic m1receptors but had no effect on actions of F6. These results demonstrate that anesthetics and a nonanesthetic inhibit the function of muscarinic m1receptors and suggest activation of protein kinase C as the mechanism of action of anesthetics and ethanol on these receptors.
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