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ATP-mediated potassium recycling in the cochlear supporting cells

ATP-mediated potassium recycling in the cochlear supporting cells Gap junction-mediated K+ recycling in the cochlear supporting cell has been proposed to play a critical role in hearing. However, how potassium ions enter into the supporting cells to recycle K+ remains undetermined. In this paper, we report that ATP can mediate K+ sinking to recycle K+ in the cochlear supporting cells. We found that micromolar or submicromolar levels of ATP could evoke a K+-dependent inward current in the cochlear supporting cells. At negative membrane potentials and the resting membrane potential of −80 mV, the amplitude of the ATP-evoked inward current demonstrated a linear relationship to the extracellular concentration of K+, increasing as the extracellular concentration of K+ increased. The inward current also increased as the concentration of ATP was increased. In the absence of ATP, there was no evoked inward current for extracellular K+ challenge in the cochlear supporting cells. The ATP-evoked inward current could be inhibited by ionotropic purinergic (P2X) receptor antagonists. Application of pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, 50 µM) or pre-incubation with an irreversible P2X7 antagonist oxidized ATP (oATP, 0.1 mM) completely abolished the ATP-evoked inward current at the negative membrane potential. ATP also evoked an inward current at cell depolarization, which could be inhibited by intracellular Cs+ and eliminated by positive holding potentials. Our data indicate that ATP can activate P2X receptors to recycle K+ in the cochlear supporting cells at the resting membrane potential under normal physiological and pathological conditions. This ATP-mediated K+ recycling may play an important role in the maintenance of cochlear ionic homeostasis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Purinergic Signalling Springer Journals

ATP-mediated potassium recycling in the cochlear supporting cells

Purinergic Signalling , Volume 6 (2) – May 18, 2010

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References (45)

Publisher
Springer Journals
Copyright
Copyright © 2010 by Springer Science+Business Media B.V.
Subject
Biomedicine; Cancer Research ; Neurosciences ; Human Physiology ; Pharmacology/Toxicology ; Biomedicine general
ISSN
1573-9538
eISSN
1573-9546
DOI
10.1007/s11302-010-9184-9
pmid
20806014
Publisher site
See Article on Publisher Site

Abstract

Gap junction-mediated K+ recycling in the cochlear supporting cell has been proposed to play a critical role in hearing. However, how potassium ions enter into the supporting cells to recycle K+ remains undetermined. In this paper, we report that ATP can mediate K+ sinking to recycle K+ in the cochlear supporting cells. We found that micromolar or submicromolar levels of ATP could evoke a K+-dependent inward current in the cochlear supporting cells. At negative membrane potentials and the resting membrane potential of −80 mV, the amplitude of the ATP-evoked inward current demonstrated a linear relationship to the extracellular concentration of K+, increasing as the extracellular concentration of K+ increased. The inward current also increased as the concentration of ATP was increased. In the absence of ATP, there was no evoked inward current for extracellular K+ challenge in the cochlear supporting cells. The ATP-evoked inward current could be inhibited by ionotropic purinergic (P2X) receptor antagonists. Application of pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, 50 µM) or pre-incubation with an irreversible P2X7 antagonist oxidized ATP (oATP, 0.1 mM) completely abolished the ATP-evoked inward current at the negative membrane potential. ATP also evoked an inward current at cell depolarization, which could be inhibited by intracellular Cs+ and eliminated by positive holding potentials. Our data indicate that ATP can activate P2X receptors to recycle K+ in the cochlear supporting cells at the resting membrane potential under normal physiological and pathological conditions. This ATP-mediated K+ recycling may play an important role in the maintenance of cochlear ionic homeostasis.

Journal

Purinergic SignallingSpringer Journals

Published: May 18, 2010

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