乙酰胆碱对大鼠皮质神经元瞬时外向钾通道的调控作用

BACKGROUND： The neuronal transient outward potassium channel has been shown to be highly associated with acetylcholine. However, the influence of acetylcholine on the transient outward potassium current in cerebral cortical neurons remains poorly understood. OBJECTIVE： To investigate acetylcholine modulation on transient outward potassium current in rat parietal cortical neurons using the whole-cell patch-clamp technique. DESIGN, TIME AND SETTING： A neuroelectrophysiology study was performed at the Department of Physiology, Harbin Medical University between January 2005 and January 2006. MATERIALS： Wistar rats were provided by the Animal Research Center, the Second Hospital of Harbin Medical University; PC-IIC patch-clamp amplifier and IBBClamp data collection analysis system were provided by Huazhong University for Science and Technology, Wuhan, China; PP-83 microelectrode puller was purchased from Narrishage, Japan. METHODS： The parietal somatosensory cortical neurons were acutely dissociated, and the modulation of acetylcholine （0.1, 1, 10, 100 μmol/L） on transient outward potassium channel was recorded using the whole-cell patch-clamp technique. MAIN OUTCOME MEASURES： Influence of acetylcholine on transient outward potassium current, potassium channel activation, and inactivation. RESULTS： The inhibitory effect of acetylcholine on transient outward potassium current was dose- and voltage-dependent （P 〈 0.01）. Acetylcholine was found to significantly affect the activation process of transient outward potassium current, i.e., the activation curve of transient outward potassium current was left-shifted, while the inactivation curve was shifted to hyperpolarization. Acetylcholine significantly prolonged the time constant of recovery from inactivation of transient outward potassium current （P 〈 0.01）. CONCLUSION： These results suggest that acetylcholine inhibits transient outward potassium current by regulating activation and inactivation processes of the transient outward potassium channel.

Acetylcholine modulates transient outward potassium channel in acutely isolated cerebral cortical neurons of rats

BACKGROUND:The neuronal transient outward potassium channel has been shown to be highly associated with acetylcholine.However,the influence of acetylcholine on the transient outward potassium current in cerebral cortical neurons remains poorly understood.OBJECTIVE:To investigate acetylcholine modulation on transient outward potassium current in rat parietal cortical neurons using the whole-cell patch-clamp technique.DESIGN,TIME AND SETTING:A neuroelectrophysiology study was performed at the Department of Physiology,Harbin Medical University between January 2005 and January 2006.MATERIALS:Wistar rats were provided by the Animal Research Center,the Second Hospital of Harbin Medical University;PC-IIC patch-clamp amplifier and IBBClamp data collection analysis system were provided by Huazhong University for Science and Technology,Wuhan,China;PP-83 microelectrode puller was purchased from Narrishage,Japan.METHODS:The parietal somatosensory cortical neurons were acutely dissociated,and the modulation of acetylcholine (0.1,1,10,100 μmol/L) on transient outward potassium channel was recorded using the whole-cell patch-clamp technique.MAIN OUTCOME MEASURES:Influence of acetylcholine on transient outward potassium current,potassium channel activation,and inactivation.RESULTS:The inhibitory effect of acetylcholine on transient outward potassium current was dose- and voltage-dependent (P<0.01).Acetylcholine was found to significantly affect the activation process of transient outward potassium current,i.e.,the activation curve of transient outward potassium current was left-shifted,while the inactivation curve was shifted to hyperpolarization.Acetylcholine significantly prolonged the time constant of recovery from inactivation of transient outward potassium current (P<0.01).CONCLUSION:These results suggest that acetylcholine inhibits transient outward potassium current by regulating activation and inactivation processes of the transient outward potassium channel.