Effect of ZnCl2 and Chelation of Zinc Ions by N,N-Diethyldithiocarbamate (DEDTC) on the ERG b-Wave Amplitude from the Isolated Superfused Vertebrate Retina

Abstract

Purpose: NiCl2 (15 µM) enhances the ERG b-wave amplitude of vertebrate retina, up to 1.5-fold by blocking E/R-type voltage-gated Ca2+ channels, which is mediated by blocking the release of GABA onto ionotropic GABA-A and GABA-C receptors. In vivo, it is likely that zinc, rather than nickel ions, may be involved in the modulation of retinal signalling. Therefore, we tested the effect of both, ZnCl2 (10 to 500 µM) and DEDTC (100 to 500 µM), which chelates zinc ions for the capacity to influence the ERG b-wave amplitude.Methods: Transretinal potentials from the isolated bovine retina were recorded as electroretinograms and Ca2+ inward currents by patch-clamp recordings of stably Cav2.3 transfected HEK-293 cells, yielding an IC50 value of 5.3 µM for ZnCl2.Results: ZnCl2 (10–15 µM) increased the b-wave amplitude by 1.52-fold ± 0.12 (n = 6 retinas), which was partially reversible upon washout. The same 1.5-fold stimulation of the b-wave amplitude was reported recently for 15 µM NiCl2. The superfusion of isolated retinas by DEDTC (100 µM) caused a transient decrease of the ERG b-wave amplitude (0.75-fold ± 0.06; n = 4), suggesting that the co-secretion of Zn2+ ions may occur under scotopic conditions.Conclusion: The stimulatory effect of ZnCl2 on the ERG b-wave amplitude resembles the stimulatory effect of NiCl2 and may be mediated rather by the NiCl2-sensitive, Cav2.3 E-/R-type voltage-gated Ca2+ channels than by NiCl2-sensitive T-type channels.