A glutamate-activated chloride current in cone-driven ON bipolar cells of the white perch retina

Abstract

Cone-driven ON-type bipolar cells were patch clamped in white perch retinal slices. Application of glutamate activated a current (I(Glu)) that was mediated by a conductance increase. The reversal potential for I(Glu) followed E(Cl) closely when the intracellular chloride concentration was varied. I(Glu) was not blocked by 100 μM picrotoxin or 1 μM strychnine, indicating that it was not caused by inhibitory input. I(Glu) is not mediated by a typical ionotropic glutamate receptor since it was not activated by kainate, AMPA, or NMDA, or blocked by kynurenic acid, CNQX, DNQX, or AP-V. Further, I(Glu) is not mediated by a known metabotropic glutamate receptor since it was not activated by quisqualic acid, AP-4, ACPD, or ibotenate. I(Glu) required the presence of extracellular sodium and could be partially inhibited by the glutamate uptake inhibitors THA and tPDC. This is suggestive of sodium-dependent glutamate transport. However, when intracellular sodium was greatly increased, neither the magnitude nor reversal potential of I(Glu) was substantively affected. Thus, I(Glu) appears to involve a chloride channel activated by a glutamate receptor with transporter-like pharmacology. I(Glu) is localized to the dendrites of the bipolar cell, where bipolar cells receive an endogenous glutamatergic input from photoreceptors. Further, the reversal potential of the light response in these cells is the same as that of I(Glu). Thus, it seems likely that I(Glu) is the current responsible for the cone component of the ON bipolar cell light response in the teleost retina.