Open AccessDopamine D2 Receptor-Mediated Modulation of Rat Retinal Ganglion Cell Excitability
Author(s) -
Ning Yin,
Yulong Yang,
Shuo Cheng,
Hongning Wang,
Xin Hu,
Yanying Miao,
Fang Li,
Zhongfeng Wang
Publication year - 2019
Publication title -
neuroscience bulletin/neuroscience bulletin
Language(s) - English
Resource type - Journals
eISSN - 1673-7067
pISSN - 1995-8218
DOI - 10.1007/s12264-019-00431-3
Subject(s) - quinpirole , dopamine receptor d2 , protein kinase a , chemistry , agonist , dopamine receptor , microbiology and biotechnology , biology , neuroscience , dopamine , receptor , kinase , biochemistry
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 cAMP/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.