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在新鲜分离的神经细胞模型上,运用制霉菌素(nystatin)穿孔膜片钳方法研究α_2及5-HT_2与甘氨酸受体之间对话的分子机理。发现:刺激α_2受体,抑制腺苷酸环化酶,减少cAMP的生成,使PKA活性降低,从而增强甘氨酸受体的功能;刺激5-HT_2受体,激活磷脂酶C(PLC),增加甘油二醋(DAG)的生成。DAG增强不依赖Ca~(2+)的新型PKC(nPKC)的活性,从而增强甘氨酸受体的功能,α_2及5-HT_2受体与甘氨酸受体之间的对话具有重要的生理意义。
In freshly isolated neural cell models, the molecular mechanism of the conversions between α 2 and 5-HT 2 and glycine receptors was investigated using the nystatin perforated patch-clamp method. It was found that stimulation of α_2 receptor, inhibition of adenylate cyclase, reduction of cAMP production and decrease of PKA activity enhanced the function of glycine receptors; stimulation of 5-HT_2 receptor, activation of phospholipase C (PLC), increase of glycerol The formation of two vinegar (DAG). DAG enhances the activity of a novel PKC (nPKC) that is independent of Ca 2+, thereby enhancing the function of glycine receptors. The dialogue between α 2 and 5-HT 2 receptors and glycine receptors has important physiological significance.