April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Calcium-Dependence of Calcium-Activated Chloride Channels in Rod Photoreceptors
Author Affiliations & Notes
  • A. Mercer
    Ophthalmology & Visual Sciences, University of Nebraska Medical Center, Omaha, Nebraska
  • K. Rabl
    Ophthalmology, University of California San Francisco, San Francisco, California
  • W. B. Thoreson
    Ophthalmology & Visual Sciences, University of Nebraska Medical Center, Omaha, Nebraska
  • Footnotes
    Commercial Relationships  A. Mercer, None; K. Rabl, None; W.B. Thoreson, None.
  • Footnotes
    Support  Research to Prevent Blindness and NIH EY10542
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1009. doi:
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      A. Mercer, K. Rabl, W. B. Thoreson; Calcium-Dependence of Calcium-Activated Chloride Channels in Rod Photoreceptors. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1009.

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

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Purpose: : Calcium-activated chloride channels are localized to synaptic terminals of rods. Chloride efflux through Ca2+-activated chloride channels inhibits L-type Ca2+ channels. We examined the Ca2+-dependence of Ca2+-activated chloride channels and their proximity to Ca2+ channels in the photoreceptor terminal.

Methods: : Whole cell recordings were obtained from rods in the tiger salamander retinal slice preparation. ECl in the pipette solutions was -20 mV. Intracellular Ca2+ was measured on a confocal microscope using Oregon Green 488 BAPTA-6F introduced into the cell through the patch pipette.

Results: : Flash photolysis of DM-nitrophen abruptly elevated Ca2+and evoked rapidly activating inward currents in rods that exhibited a Kd for Ca2+ of 437 nM (N=31). Depolarizing steps evoked long-lasting tail currents that could be inhibited by niflumic acid and reversed near ECl, indicating that they were due to activation of Ca2+-activated chloride channels. To analyze the distance from Ca2+ channels to Ca2+-activated chloride channels, we compared effects on tail currents of fast (5 mM BAPTA) and slow (0.5 or 5 mM EGTA) Ca2+ buffers introduced into the photoreceptor terminal through the patch pipette. After waiting >10 min. for chelators to diffuse to the terminal, tail currents evoked by 500 ms steps to -10 mV averaged 429.0 ± 49.1 pA with 0.5 mM EGTA (N=11), 187.4 ± 41.1 pA with 5 mM EGTA (N=5), and 80.25 ± 25.4 pA with 5 mM BAPTA (N=9). By comparing these results with the profile of free Ca2+ predicted to surround a Ca2+ channel in the presence of the different buffers, we estimate that Ca2+-activated Cl- channels are an average of ~360 nm from Ca2+ channels.

Conclusions: : We find that Ca2+-activated Cl- channels can be activated by submicromolar Ca2+ levels and are located a few hundred nm from Ca2+ channels. By comparison, effects of presynaptic BAPTA and EGTA on post-synaptic currents evoked in horizontal cells by presynaptic stimulation of rods suggest that synaptic release sites are less than 100 nm from Ca2+ channels.

Keywords: photoreceptors • ion channels • synapse 

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