April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Zinc Modulation of L-type Calcium Channels at Photoreceptor Terminals
Author Affiliations & Notes
  • Ivan Anastassov
    Biology, Hunter College & Graduate Center CUNY, New York, New York
    MBL, Woods Hole, Massachusetts
  • Wen Shen
    MBL, Woods Hole, Massachusetts
    Florida Atlantic University, Boca Raton, Florida
  • Harris Ripps
    MBL, Woods Hole, Massachusetts
    Ophthalmology & Visual Science, University of Illinois at Chicago, Chicago, Illinois
  • Richard Chappell
    Biology, Hunter College & Graduate Center CUNY, New York, New York
    MBL, Woods Hole, Massachusetts
  • Footnotes
    Commercial Relationships  Ivan Anastassov, None; Wen Shen, None; Harris Ripps, None; Richard Chappell, None
  • Footnotes
    Support  NSF #1026531; NCRR/NIH #RR003037; (RLC).
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4802. doi:
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      Ivan Anastassov, Wen Shen, Harris Ripps, Richard Chappell; Zinc Modulation of L-type Calcium Channels at Photoreceptor Terminals. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4802.

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

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Purpose: : To determine whether the release of endogenous zinc acts to modulate calcium channels at the photoreceptor terminal.

Methods: : Photoreceptor cells were isolated from tiger salamander (Ambystoma tigrinium) retina. Light-adapted photoreceptors were loaded with the calcium indicator dye Fluo-4,AM. Calcium influx was initiated by depolarization with 30mM KCl. Changes in dye intensity were recorded with a Zeiss fluorescence microscope to reveal differences in [Ca 2+ ]i. Drugs were delivered via a pressure perfusion system with fast, valve-controlled solution changes. Images were taken every second (exposure time=150ms). An average decay curve of peak fluorescence intensity with time was obtained from repeated applications of 30mM KCl alone. Trials started with a control application of KCl alone and subsequent responses were normalized to the first peak.

Results: : Application of 2 mM Zn 2+ resulted in an 88% reduction in Ca 2+ influx and was reversible. The L-type Ca 2+ channel blockers nicardipine and verapamil (50-100uM) produced a similar reduction in Ca 2+ influx. Chelation of endogenously released Zn 2+ with the membrane-impermeable chelator histidine (10mM) increased the Ca 2+ influx by 51%. Application of Zn 2+ together with histidine recovered 23% of the Ca 2+ signal. The enhancing effect on the Ca 2+ current by the Zn 2+ chelator histidine was blocked with both nicardipine and verapamil.

Conclusions: : The co-release of ionic Zn 2+ and glutamate at rod photoreceptor terminals was shown previously. Here, we show that exogenous ionic Zn 2+ is a potent, but reversible blocker of L-type Ca 2+ channels at the cone photoreceptor terminal. The action of Zn 2+ at these channels was mimicked by the Ca 2+ channel blockers nicardipine and verapamil; their effect, however, was not as readily reversible. More importantly, chelation of endogenously released Zn 2+ by histidine resulted in the relief of inhibition on L-type Ca 2+ channels and led to an increase in Ca 2+ influx. Thus, the concentration of Zn 2+ co-released with glutamate, under normal physiological conditions, serves an important modulatory role at the photoreceptor terminal.

Keywords: calcium • photoreceptors • imaging/image analysis: non-clinical 

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