Abstract

The effects of Zn 2+ on color-opponent bipolar cells (BCs) and amacrine cells (ACs) were studied in the isolated superfused carp retina using intracellular recording techniques. Bath-applied Zn 2+ (25 μM) depolarized R +G −-type BCs and suppressed both depolarizing responses of these cells to red (680 nm) flashes and hyperpolarizing ones to green (500 nm) flashes. Following Zn 2+ application, G +R −-type BCs were hyperpolarized, which was accompanied by a potentiation of their depolarizing responses to green flashes and a suppression of hyperpolarizing ones to red flashes. Similar Zn 2+ effects were observed in R +G −- and G +R −-type ACs. The Zn 2+ effects persisted in the presence of picrotoxin and strychnine, suggesting that modulation by Zn 2+ of GABA and glycine receptors was unlikely involved. Using whole-cell recording techniques, it was found Ca 2+ currents in cone terminals were dose-dependently suppressed by Zn 2+, suggesting that Zn 2+ may reduce glutamate release from cone photoreceptors. Furthermore, lowering extracellular Ca 2+, a procedure that increases glutamate release from photoreceptors, exerted actions on R +G −- and G +R −-type BCs, almost opposite to the Zn 2+ effects on these two types of BCs. It is therefore postulated that the Zn 2+ effects reported in the present work may reflect a consequence of the changes in input resistances of color-opponent BCs and driving forces for their light responses resulted from the reduced glutamate release by Zn 2+.

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