Activation of group I metabotropic glutamate receptors regulates the excitability of rat retinal ganglion cells by suppressing Kir and Ih
Qian Li; Peng Cui; Yanying Miao; Feng Gao; Xue-Yan Li; Wen-Jing Qian; Shu-Xia Jiang; Xing-Huai Sun; Zhongfeng Wang
2017-07
会议名称2017年第二届曲阜视觉科学会议
会议日期2017.7.1
会议地点曲阜
摘要

Institutes of Brain Science and Eye & ENT Hospital, State Key Laboratory of Medical Neurobiology, Shanghai Key Laboratory of Visual Impairment and Restoration, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Group I metabotropic glutamate receptor (mGluR I) activation exerts a slow postsynaptic excitatory effect in the CNS. Here, the issues of whether and how this receptor is involved in regulating retinal ganglion cell (RGC) excitability were investigated in retinal slices using patch-clamp techniques. Under physiological conditions, RGCs displayed spontaneous firing. Extracellular application of LY367385 (10 µM)/MPEP (10 µM), selective mGluR1 and mGluR5 antagonists respectively, significantly reduced the firing frequency, suggesting that glutamate endogenously released from bipolar cells constantly modulates RGC firing. DHPG (10 µM), an mGluR I agonist, significantly increased the firing and caused depolarization of the cells, which were reversed by LY367385, but not by MPEP, suggesting the involvement of the mGluR1 subtype. Intracellular Ca2+-dependent PI-PLC/PKC and calcium/calmodulin-dependent protein kinase II (CaMKII) signaling pathways mediated the DHPG-induced effects. In the presence of cocktail synaptic blockers (CNQX, D-AP5, bicuculline, and strychnine), which terminated the spontaneous firing in both ON and OFF RGCs, DHPG still induced depolarization and triggered the cells to fire. The DHPG-induced depolarization could not be blocked by TTX. In contrast, Ba2+, an inwardly rectifying potassium channel (Kir) blocker, and Cs+ and ZD7288, hyperpolarization-activated cation channel (Ih) blockers, mimicked the effect of DHPG. Furthermore, in the presence of Ba2+/ZD7288, DHPG did not show further effects. Moreover, Kir and Ih currents could be recorded in RGCs, and extracellular application of DHPG indeed suppressed these currents. Our results suggest that activation of mGluR I regulates the excitability of rat RGCs by inhibiting Kir and Ih.

关键词mGluR I excitability spontaneous firing Kir Ih retinal ganglion cell
学科领域视觉神经科学
语种英语
文献类型会议论文
条目标识符http://ir.psych.ac.cn/handle/311026/22052
专题心理所主办学术会议_2017年第二届曲阜视觉科学会议_会议摘要
作者单位1.Institutes of Brain Science and Eye & ENT Hospital
2.State Key Laboratory of Medical Neurobiology
3.Key Laboratory of Visual Impairment and Restoration, Collaborative Innovation Center for Brain Science, Fudan University
推荐引用方式
GB/T 7714
Qian Li,Peng Cui,Yanying Miao,et al. Activation of group I metabotropic glutamate receptors regulates the excitability of rat retinal ganglion cells by suppressing Kir and Ih[C],2017.
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