• Top page
  • Timetable
  • Per session
  • Per presentation
  • How to
  • Meeting Planner



Ion Channels and Excitable Membranes

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Modulation by ATP of glycine receptors in rat retinal ganglion cells

  • P1-013
  • Pingping Zhang:1 Yi-Yang Li:1,2,3,4 Shi-Jun Weng:1,2,3,4 Xiong-Li Yang:1,2,3,4 Yong-Mei Zhong:1,2,3,4 
  • 1:Fudan University 2:Institute of Neurobiology 3: Institutes of Brain Science  4:State Key Laboratory of Medical Neurobiology 

As a neurotransmitter in the central nervous system, adenosine triphosphate (ATP) functions by acting on two distinct subfamilies of purinoceptors: seven ionotropic P2X receptors and eight metabotropic mammalian P2Y receptors. It has been shown that ATP is present in the retina and P2Y receptors are expressed in a variety of retinal neurons, especially in retinal ganglion cells (GCs). In the present work, by using whole-cell patch clamp techniques in rat retinal slice preparations, we investigated modulation by ATP of current responses mediated by glycine receptors of GCs. Bath application of ATP suppressed glycine- and light-induced glycine receptor-mediated currents of GCs, but the degradation product of ATP adenosine did not. When the degradation of ATP was blocked by the ectonucleotidase antagonist ARL67156, ATP persisted to suppress glycine currents of GCs. The ATP effect was not changed by co-application of Evans Blue, a P2X receptor antagonist, suggesting no involvement of P2X receptors. In contrast, the ATP-induced suppression of glycine currents was abolished by P2 receptor antagonists (pyridoxal-phosphate-6-azophenyl-2', 4'-disulphonic acid and suramine) and GDP-β-S, suggesting the involvement of G-protein coupled P2Y receptors. Specifically, the ATP effect was in part eliminated by perfusion of MRS2500, a selective P2Y1R antagonist or NF157, a selective P2Y11 antagonist. These results suggest that ATP suppresses glycine receptors of GCs via activation of P2Y1 and P2Y11 receptors.

This work was supported by the grants from the National Program of Basic Research sponsored by the Ministry of Science and Technology of China (2011CB504602), the National Natural Science Foundation of China (31070967, 31171055, 30930034, 31121061).

Copyright © Neuroscience2014. All Right Reserved.