A GLUTAMATE-ACTIVATED CHLORIDE CURRENT IN CONE-DRIVEN ON BIPOLAR CELLS OF THE WHITE PERCH RETINA

Cone-driven ON-type bipolar cells were patch clamped in white perch re tinal slices, Application of glutamate activated a current (I-Glu) tha t was mediated by a conductance increase, The reversal potential for I -Glu followed E(Cl) closely when the intracellular chloride concentrat ion was varied. I-Glu was not blocked by 100 mu M picrotoxin or 1 mu M strychnine, indicating that it was not caused by inhibitory input, I- Glu is not mediated by a typical ionotropic glutamate receptor since i t 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 quisqual ic acid, AP-4, ACPD, or ibotenate. I-Glu required the presence of extr acellular sodium and could be partially inhibited by the glutamate upt ake inhibitors THA and tPDC. This is suggestive of sodium-dependent gl utamate transport, However, when intracellular sodium was greatly incr eased, neither the magnitude nor reversal potential of I-Glu was subst antively affected. Thus, I-Glu appears to involve a chloride channel a ctivated by a glutamate receptor with transporter-like pharmachology. 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 i s the same as that of I-Glu. Thus, it seems likely that I-Glu is the c urrent responsible for the cone component of the ON bipolar cell light response in the teleost retina.