Gb. Grant et Je. Dowling, A GLUTAMATE-ACTIVATED CHLORIDE CURRENT IN CONE-DRIVEN ON BIPOLAR CELLS OF THE WHITE PERCH RETINA, The Journal of neuroscience, 15(5), 1995, pp. 3852-3862
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.