Zn(2+) modulates light responses of color-opponent bipolar and amacrine cells in the carp retina.

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 micro M) 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+).