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

The effects of Zn2+ were studied while recording intracellularly from L-type horizontal cells (LHCs) in the isolated, superfused carp retina. In darkness, 25 microM 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 gamma-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.