May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
The creatine kinase/phosphocreatine system modulates oscillations in WFACs.
Author Affiliations & Notes
  • A. Gross
    Ophthalamogy, Univ Utah–Moran Eye Center, Salt Lake City, UT
  • J. Vigh
    Vollum Institute, OHSU, Portland, OR
  • K. Rapp
    Ophthalamogy, Univ Utah–Moran Eye Center, Salt Lake City, UT
  • E.M. Lasater
    Ophthalamogy, Univ Utah–Moran Eye Center, Salt Lake City, UT
  • Footnotes
    Commercial Relationships  A. Gross, None; J. Vigh, None; K. Rapp, None; E.M. Lasater, None.
  • Footnotes
    Support  NIH Grant EY 05972 and Research to Prevent Blindness, Inc.
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 4265. doi:
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      A. Gross, J. Vigh, K. Rapp, E.M. Lasater; The creatine kinase/phosphocreatine system modulates oscillations in WFACs. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4265.

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

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Abstract: : Purpose: The creatine kinase/phosphocreatine system has been shown to regulate ion channels. In wide–field amacrine cells (WFACs) in the teleost white bass the interplay between voltage–dependent Ca (ICa) and calcium dependent potassium (KCa) currents generates membrane potential oscillations. The aim of this study was to test the hypothesis that creatine phosphokinase is involved in the regulation of the oscillatory behavior of WFACs Methods: Recordings were obtained from WFACs using standard whole cell voltage clamp. The cells were held at –70mV for both the current–and voltage clamp protocols. To examine the Ca currents, the cells were bathed in Ringer's containing 2.1mM Ca2+ with potassium and sodium blockers. Creatine phosphokinase was applied through the recording pipette with or without MgATP and/or creatinephosphate. Results: Under control conditions (2.1mM extracellular Ca2+) including creatine phosphokinase+MgATP+creatinephosphate in the pipette solution had no noticeable effect on the oscillations. Application of high extracellular Ca2+ (5–10mM) after a transient enhancement inhibited the oscillations. However, in the presence of the kinase+MgATP the enhacement of the oscillations were more pronounced and sustained. Analysis of the ICa revealed a substantial decrease in the amplitude induced by the kinase. Conclusions: Creatine phosphokinase activity is responsible for the decrease of ICa, consequently lessening the Ca–dependent inactivation of ICa thereby increasing the oscillations. The KCa currents are also influenced so that the membrane potential remains in the optimal range for oscillatory behaviour. It is possible that oscillatory behavior is linked to energy metabolism in WFACs. The creatine phosphokinase may play a critical role during transient metabolic increases to adjust conductance of voltage–gated Ca and K(Ca) channels for optional information processing.

Keywords: amacrine cells • calcium • electrophysiology: non–clinical 

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