December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Calcium-dependent Inactivation and Depletion of Synaptic Cleft Calcium Ions Regulate the Amplitude of Rod Calcium Currents Under Physiological Conditions
Author Affiliations & Notes
  • K Rabl
    Ophthalmology University of Nebraska Medical Center Omaha NE
  • WB Thoreson
    Ophthalmology University of Nebraska Medical Center Omaha NE
  • Footnotes
    Commercial Relationships   K. Rabl, None; W.B. Thoreson, None. Grant Identification: Support: NIH Grant EY10542 and Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3753. doi:
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      K Rabl, WB Thoreson; Calcium-dependent Inactivation and Depletion of Synaptic Cleft Calcium Ions Regulate the Amplitude of Rod Calcium Currents Under Physiological Conditions . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3753.

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Abstract

Abstract: : Purpose:1) To determine the degree of Ca2+-dependent inactivation of Ca2+ currents (ICa) in rods with intact endogenous Ca2+ buffers and physiological [Ca2+] and 2) to test whether sustained influx through Ca2+ channels depletes synaptic cleft Ca2+ ions sufficiently to inhibit ICa. Methods: Gramicidin perforated patch whole cell recordings were obtained from enzymatically dissociated rods and rods in retinal slices of the larval tiger salamander. Cells were perfused with 1.8 mM Ba2+ or 1.8-2.0 mM Ca2+, 10 mM TEA and 0.3 mM niflumic acid. ICa amplitude was measured using voltage ramps (0.5 mV/ms) applied before and after a 5 s depolarizing step. Results: Depolarizing rods in retinal slices to -10 mV for 5 s almost completely inhibited ICa recorded 5 s after termination of the step. Depolarizing steps to -40 mV also significantly inhibited ICa. Such inhibition of ICa in the slice could arise from both Ca2+-dependent inactivation and depletion of synaptic cleft Ca2+. To assess Ca2+-dependent inactivation in the absence of synaptic cleft depletion, we recorded from isolated rods lacking synaptic contacts. In isolated rods, depolarizing steps to -10 mV inhibited ICa by 75% and steps to -40 mV inhibited ICa by 20%. Replacing Ca2+ with Ba2+ reduces Ca2+-dependent inactivation; IBa in isolated rods was inhibited only 25% by 5 s steps to -10 mV and <10% by steps to -40 mV. In contrast, IBa recorded from rods in the slice with 1.8 mM Ba2+ was inhibited 50% after a step to -10 mV and 25% after a step to -40 mV. The greater inhibition of IBa produced by depolarizing steps in the retinal slice compared to isolated rods is likely due to synaptic cleft depletion. Conclusion: In the presence of endogenous Ca2+ buffers and physiological Ca2+ levels, Ca2+-dependent inactivation inhibited ICa by 75% following a step to -10 mV. In cells with synaptic terminals, synaptic cleft depletion can inhibit ICa an additional 25%. The sum of these two mechanisms almost complete inhibits ICa following a 5 s step to -10 mV in the retinal slice. This potent inhibition may help prevent excessive activation of ICa in photoreceptors. Inhibitory effects of steps to -40 mV suggest that these mechanisms may also help regulate ICa and thus synaptic transmission around the dark resting potential of rods.

Keywords: 334 calcium • 594 synapse • 517 photoreceptors 
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