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目的和方法：本研究采用全细胞膜片箝技术，观察皮质酮（Ｂ）对ＰＣ１２细胞上乙酰胆碱诱发电流（ＩＡＣｈ）的快速作用并初步探讨其可能机制。结果：ＰＣ１２细胞上ＩＡＣｈ是通过烟碱受体（ｎＡＣｈＲ）引起的。箝制电压为－８０ｍＶ时，ＡＣｈ（３０μｍｏｌ／Ｌ）诱发一内向电流；细胞外灌流同时给予ＡＣｈ和Ｂ（１０－５ｍｏｌ／Ｌ）时，Ｂ对ＩＡＣｈ的抑制作用较弱；用Ｂ（１０－５ｍｏｌ／Ｌ）对细胞进行预处理，可提高Ｂ对ＩＡＣｈ峰值的抑制率，作用呈可逆性、浓度依赖性和非电压依赖性；细胞外用ＲＮＡ合成抑制剂放线菌素Ｄ（４×１０－５～４×１０－３ｍｏｌ／Ｌ）或蛋白合成抑制剂放线菌酮（１０－４～１０－３ｍｏｌ／Ｌ）孵育细胞１～２ｈ阻断基因机制，但均不影响Ｂ对ＩＡＣｈ的快速抑制作用。结论：Ｂ对ＰＣ１２细胞上ＩＡＣｈ有快速抑制作用，此作用可能是由非基因组机制介导的。
PURPOSE AND METHODS: Whole-cell patch-clamp technique was used in this study to observe the rapid effect of corticosterone (BAC) on acetylcholine-induced current (IACh) in PC12 cells and to explore its possible mechanism. RESULTS: IACh on PC12 cells was caused by nicotinic receptor (nAChR). When the clamping voltage was -80mV, ACh (30μmol / L) induced an inward current; when ACh and B (10-5mol / L) were administered by extracellular perfusion, the inhibitory effect of B on IACh was weak; / L) pretreatment could increase the inhibitory rate of B to IACh peak, and the effect was reversible, concentration-dependent and voltage-independent. Extracellular RNA synthesis inhibitor actinomycin D (4 × 10-5 ~ 4 × 10-3mol / L) or cycloheximide (10-4 ~ 10-3mol / L) for 1 ~ 2h. However, they did not affect the rapid inhibitory effect of B on IACh . Conclusion: B has a rapid inhibitory effect on IACh in PC12 cells, which may be mediated by non-genomic mechanisms.