Abstract
The effects of Zn 2+ were studied while recording intracellularly from L-type horizontal cells (LHCs) in the isolated, superfused carp retina. In darkness, 25 μM Zn 2+ hyperpolarized LHCs and potentiated responses of these cells to 500 nm flashes, but decreased those to 680 nm flashes. Zn 2+ did not change photopic electroretinographic P III responses. The differential modulation by Zn 2+ persisted when the Zn 2+-induced membrane hyperpolarization was compensated by lowering Ca 2+ 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 Zn 2+. Decreased glutamate release from the cone terminal by Zn 2+ results in a reduction of cone signals. Zn 2+ antagonizes GABA receptors on LHCs, leading to cone signal reduction. On the other hand, Zn 2+ 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 Zn 2+-induced feedback strength change may account for the differential modulation.
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