April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Downregulation of Inward Rectifying Potassium Channels (Kir) by Activation of Group I mGluRs in Rat Retinal Müller Cells
Author Affiliations & Notes
  • M. Ji, IV
    Institute of Neurobiology and Eye & ENT Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China
  • X.-H. Sun
    Institute of Neurobiology and Eye & ENT Hospital,Fudan University, Shanghai, China
  • X.-L. Yang
    Institutes of Brain Science and State Key Laboratory of Medical Neurobiology,Fudan University, Shanghai, China
  • Z.-F. Wang
    Institutes of Brain Science and State Key Laboratory of Medical Neurobiology,Fudan University, Shanghai, China
  • Footnotes
    Commercial Relationships  M. Ji, IV, None; X.-H. Sun, None; X.-L. Yang, None; Z.-F. Wang, None.
  • Footnotes
    Support  China "973" 2007CB512200
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5755. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M. Ji, IV, X.-H. Sun, X.-L. Yang, Z.-F. Wang; Downregulation of Inward Rectifying Potassium Channels (Kir) by Activation of Group I mGluRs in Rat Retinal Müller Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5755.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : Glutamate is a major excitatory neurotransmitter in the mammalian retina. In the present work, we aimed to determine the modulation effect of glutamate on inward rectifying potassium channels (Kir) in rat retinal Müller cells and to explore the possible intracellular signaling pathway.

Methods: : Müller cells were freshly dissociated from adult male Sprague-Dawley rats by enzymatic and mechanical methods. Whole-cell currents were recorded using the patch-clamp techniques.

Results: : The Kir currents were first identified in rat retinal Müller cells. The current-voltage relationship of currents showed inward rectified. The currents were blocked by Ba2+ and the current amplitudes changed with extracellular K+ concentrations. External application of DHPG (10 µM), a selective group I metabotropic glutamate receptors (mGluRs) agonist, significantly inhibited the peak amplitudes of Kir currents, which was reversed by co-application of MPMQ (10 µM), an mGluR I antagonist. Internal dialysis of GDP-β-S (3 mM) eliminated the effect of DHPG on Kir currents. The DHPG effect was also blocked by application of U73122 (10 µM), a PI-PLC inhibitor, or haperin (5 mg/ml), an intracellular IP3 receptor antagonist. Furthermore, external application of chelerythrine chloride (5 µM), a PKC inhibitor, suppressed the DHPG effect. When intracellular Ca2+ was chelated by BAPTA (10 mM), the DHPG effect was disappeared. In contrast, PKA signaling pathway seemed not to be involved since forskolin (5 µM), a PKA activator, or Rp-cAMP (20 µM), a PKA inhibitor, had no effect on DHPG induced suppression of Kir currents.

Conclusions: : Activation of group I mGluRs suppressed Kir currents through intracellular PI-PLC/IP3/PKC signaling pathway in rat retinal Müller cells.

Keywords: Muller cells • retina • ion channels 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×