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R. L. Chappell, H. Ripps, S. Redenti; Zinc Release From Individual Photoreceptor Terminals Is Induced by Depolarization and by Black Widow Spider Venom. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5956.
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Histological studies have provided evidence for the availability of reactive zinc (Zn2+) in the region of photoreceptor terminals in a variety of species. Enhancement of the b-wave potential in response to chelation of extracellular zinc is consistent with a role for Zn2+ in information processing in the distal retina. The present study investigates the hypothesis that zinc is released from the terminals of photoreceptors in response to depolarization or by drug-induced vesicular release.
Rod photoreceptors were enzymatically isolated from zebrafish (Danio rerio) retinas and observed using confocal microscopy. During live imaging, isolated photoreceptors were exposed to either the membrane permeable or impermeable forms of the zinc-specific dye Newport Green. KCl application was used to depolarize the isolated cells. Alternatively, the imaged photoreceptors were exposed to the black widow spider venom derivative α-latrotoxin, known to induce prolonged exocytosis.
Using the membrane permeant form of the zinc-specific dye Newport green, we found evidence for bioavailable zinc inside isolated zebrafish rods throughout their length. When the rods were exposed to the membrane impermeant form of Newport green, faint staining could be observed in the photoreceptor terminal region. However, upon addition of 25 mM KCl to the bathing medium, sufficient to depolarize the cells by ~10 mV, there was a marked increase in extracellular zinc on - and adjacent to- the synaptic terminals, but not elsewhere along the elongated cells. Similar results were obtained by application of the black widow spider venom derrivative α-latrotoxin (0.5 nM). α-latrotoxin-induced zinc release from photoreceptor terminals was even more sustained, consistent with the prolonged vesicular exocytosis with which it is associated.
These findings provide direct evidence for the release of bioavailable zinc from terminals of vertebrate photoreceptors during depolarization and venom-induced vesicular exocytosis. Consequently, we suggest that zinc release from photoreceptor terminals is likely to play a role in the processing of visual information at a variety of sites, including those where zinc sensitivity has already been demonstrated, especially in the distal retina.
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