Dopamine D2 Receptor-Mediated Modulation of Rat Retinal Ganglion Cell Excitability  

作　　者：Ning Yin Yu-Long Yang Shuo Cheng Hong-Ning Wang Xin Hu Yanying Miao Fang Li Zhongfeng Wang 

机构地区：[1]Department of Neurology,State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science,Institutes of Brain Science,Zhongshan Hospital,Fudan University,Shanghai 200032,China

出　　处：《Neuroscience Bulletin》2020年第3期230-242,共13页神经科学通报（英文版）

基　　金：the National Natural Science Foundation of China(31671078,81790642,and 31872765);the Shanghai Municipal Science and Technology Major Project(No.2018SHZDZX01)and ZJ Lab.

摘　　要：Ganglion cells(RGCs) are the sole output neurons of the retinal circuity. Here, we investigated whether and how dopamine D2 receptors modulate the excitability of dissociated rat RGCs. Application of the selective D2 receptor agonist quinpirole inhibited outward K^+ currents, which were mainly mediated by glybenclamide-and 4-aminopyridine-sensitive channels, but not the tetraethylammonium-sensitive channel. In addition,quinpirole selectively enhanced Nav1.6 voltage-gated Na^+ currents. The intracellular c AMP/protein kinase A,Ca^2+/calmodulin-dependent protein kinase Ⅱ, and mitogen-activated protein kinase/extracellular signal-regulated kinase signaling pathways were responsible for the effects of quinpirole on K^+ and Na^+ currents, while phospholipase C/protein kinase C signaling was not involved. Under current-clamp conditions, the number of action potentials evoked by positive current injection was increased by quinpirole. Our results suggest that D2 receptor activation increases RGC excitability by suppressing outward K+currents and enhancing Nav1.6 currents, which may affect retinal visual information processing.

关 键 词：Retinal GANGLION cell DOPAMINE D2 receptor Outward K^+current Nav1.6 VOLTAGE-GATED Na^+current EXCITABILITY 

分 类 号：R338[医药卫生—人体生理学]