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目的:研究糖皮质激素皮质酮对PC12细胞烟碱受体的非基因组作用.方法:采用全细胞膜片箝技术记录神经生长因子分化的PC12细胞上的乙酰胆碱(ACh)诱发电流(I_(ACh)).结果:PC12细胞上I_(ACh)是由烟碱受体引起的.同时给予ACh(3Oμmol/L)和皮质酮(0.1-10μmol/L)加速I_(ACh)的衰减且轻微抑制I_(ACh)峰值.用相同浓度的皮质酮预处理细胞可加强对I_(ACh)峰值的抑制率而不影响受体失敏速率.牛血清白蛋白耦联的皮质酮(0.1-10μmol/L)对I_(ACh)有类似于皮质酮的快速抑制作用.此快速抑制作用呈可逆性、浓度依赖性和非电压依赖性.结论:皮质酮可快速抑制PC12细胞I_(ACh),已是由非基因组机制介导的.皮质酮结合于膜外的特异结合位点,很可能直接作用于神经元烟碱受体,以一种非竞争方式抑制I_(ACh),从而调控交感神经元的儿茶酚胺释放.
Objective: To study the non-genomic effect of corticosterone on nicotinic acetylcholinesterase (PCh) in PC12 cells.Methods: Whole cell patch clamp technique was used to record ACh induced current (ACh) on PC12 cells differentiated by nerve growth factor Results: I_ (ACh) on PC12 cells was induced by nicotine receptor.At the same time, ACh (30μmol / L) and corticosterone (0.1-10μmol / L) accelerated the attenuation of I_ (ACh) ) Peak.Under the same concentration of corticosterone pretreatment cells can enhance the inhibitory rate of peak I_ (ACh) without affecting the rate of receptor desensitization.Conclusion Bovine serum albumin-coupled corticosterone (0.1-10μmol / L) (ACh) had a rapid inhibition similar to corticosterone, and the rapid inhibition was reversible, concentration-dependent and voltage-independent.Conclusion: Corticosterone can rapidly inhibit I_ (ACh) in PC12 cells, which is caused by non-genomic mechanisms Mediated corticosterone binding to specific binding sites outside the membrane is likely to act directly on the neuronal nicotinic receptors in a noncompetitive manner inhibit I_ (ACh), thereby regulating the release of catecholamine sympathetic neurons.