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Ion Channels and Excitable Membranes

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

Group I metabotropic glutamate receptors regulate the excitability of rat retinal ganglion cells

  • P1-014
  • Qian Li:1 Yi Wu:1,2,3,4 Xiao-Han Wang:1,2,3,4 Xiong-Li Yang:1,2,3,4 Zhong-Feng Wang:1,2,3,4 
  • 1:Fudan University 2:Institutes of Brain Science 3:Institute of Neurobiology  4:State Key Laboratory of Medical Neurobiology 

Retinal ganglion cells (RGCs), output neurons of the retina, receive inhibitory inputs from amacrine cells and excitatory inputs directly from cone bipolar cells. Changes in RGC excitability may directly influence visual processing in the retina. Group I metabotropic glutamate receptors (mGluR I) were extensively expressed on retinal neurons. However, the effects of activating mGluR I on excitability of RGCs are largely unknown. Here, we showed that DHPG (10 μM), an mGluR I agonist, significantly increased the firing and caused a depolarization of the membrane potential of the cells, which could be reversed by LY3673845 (10 μM), a selective mGluR1 antagonist, but not by MPEP(10 μM), a selective mGluR5 antagonist. Intracellular dialysis of bisindolylmaleimide IV (10 μM), a protein kinase C inhibitor, blocked the DHPG-induced depolarization. In contrast, perfusion of KN-62 (10 μM) or KN-93(10 μM), two CaM kinaseⅡinhibitors, failed to block the DHPG effect. In the presence of cocktail synaptic blockers (CNQX, D-AP5, bicuculline and strychnine), with spontaneous firing being disappeared, DHPG persisted to depolarize the membrane potential of RGCs and induce the cells to fire action potentials, suggesting that activation of mGluR I directly regulates the excitability of RGCs. The DHPG-induced depolarization of RGCs could not be blocked by TTX, indicating no involvement of Na+ channels. In contrast, DHPG suppressed hyperpolarization-activated currents. The reverse potential of these currents was approximately -70 mV, very close to potassium equilibrium potential, implying that K+ channels were mediated the DHPG-induced effects. Further experiments showed that inwardly rectifying potassium (Kir) currents and hyperpolarization-activated cation currents (Ih) could be recorded in RGCs, and extracellular application of DHPG indeed induced suppression on these two channels. Our results suggest that activation of mGluR I may regulate the excitability of rat RGCs by suppressing Kir and Ih channels.

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