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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.
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© ARVO (1962-2015); The Authors (2016-present)
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.
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.
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.
Activation of group I mGluRs suppressed Kir currents through intracellular PI-PLC/IP3/PKC signaling pathway in rat retinal Müller cells.
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