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 retinal slices. Application of glutamate activated a current (IGlu) that was mediated by a conductance increase. The reversal potential for IGlu followed ECl closely when the intracellular chloride concentration was varied. IGlu was not blocked by 100 microM picrotoxin or 1 microM strychnine, indicating that it was not caused by inhibitory input. IGlu 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, IGlu is not mediated by a known metabotropic glutamate receptor since it was not activated by quisqualic acid, AP-4, ACPD, or ibotenate. IGlu 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 IGlu was substantively affected. Thus, IGlu appears to involve a chloride channel activated by a glutamate receptor with transporter-like pharmacology. IGlu 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 IGlu. Thus, it seems likely that IGlu is the current responsible for the cone component of the ON bipolar cell light response in the teleost retina.
Grant
G B
GB
Biological Laboratories, Harvard University, Cambridge, Massachusetts 02138, USA.
Dowling
J E
JE
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D018118:Chloride Channels / Q000187:drug effects / Q000502:physiology*; D002712:Chlorides / Q000378:metabolism; D003515:Cycloleucine / Q000031:analogs & derivatives / Q000494:pharmacology; D003712:Dendrites / Q000187:drug effects / Q000502:physiology*; D018698:Glutamic Acid / Q000494:pharmacology*; D007051:Ibotenic Acid / Q000494:pharmacology; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology; D007736:Kynurenic Acid / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D016202:N-Methylaspartate / Q000494:pharmacology; D009498:Neurotoxins / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D010471:Perches; D010852:Picrotoxin / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D016318:Quisqualic Acid / Q000494:pharmacology; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000502:physiology; D012160:Retina / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D017949:Retinal Cone Photoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D013331:Strychnine / Q000494:pharmacology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
D015763:2-Amino-5-phosphonovalerate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D018118:Chloride Channels; D002712:Chlorides; D003515:Cycloleucine; D018698:Glutamic Acid; D007051:Ibotenic Acid; D007608:Kainic Acid; D007736:Kynurenic Acid; D016202:N-Methylaspartate; D009498:Neurotoxins; D010852:Picrotoxin; D011810:Quinoxalines; D016318:Quisqualic Acid; D018094:Receptors, Metabotropic Glutamate; D013331:Strychnine; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; C036361:1-amino-1,3-dicarboxycyclopentane; C056723:FG 9041