Zn²⁺ differentially modulates signals from red- and short wavelength-sensitive cones to horizontal cells in carp retina

The effects of Zn²⁺ were studied while recording intracellularly from L-type horizontal cells (LHCs) in the isolated, superfused carp retina. In darkness, 25 μM Zn²⁺ hyperpolarized LHCs and potentiated responses of these cells to 500 nm flashes, but decreased those to 680 nm flashes. Zn²⁺ did not change photopic electroretinographic P III responses. The differential modulation by Zn²⁺ persisted when the Zn²⁺-induced membrane hyperpolarization was compensated by lowering Ca²⁺ concentration in the perfusate, but it was abolished in the presence of background illumination. Furthermore, the differential modulation no longer existed in the presence of bicuculline, suggesting the involvement of γ-aminobutyric acid_A (GABA_A) receptors. We speculate that the differential modulation may be a consequence of multiple changes caused by Zn²⁺. Decreased glutamate release from the cone terminal by Zn²⁺ results in a reduction of cone signals. Zn²⁺ antagonizes GABA receptors on LHCs, leading to cone signal reduction. On the other hand, Zn²⁺ may reduce the strength of the negative feedback from LHCs to cones by downregulating the activity of GABA receptors on the cone terminal, which causes a potentiation of LHC light responses. Cone- or wavelength-relevance of the Zn²⁺-induced feedback strength change may account for the differential modulation.