title: The role of NMDA and non-NMDA excitatory amino acid receptors in the functional organization of primate retinal ganglion cells.
abstract: The role of excitatory amino acid (EAA) receptors in primate retinal ganglion cell function was analyzed in a superfused retina-eyecup preparation using single-unit, extracellular recording techniques. The effects of bath applied L-2-amino-4-phosphonobutyrate (APB), N-methyl-D-aspartate (NMDA), and non-NMDA EAA receptor agonists and antagonists were examined on the light-evoked responses and resting firing rates of ganglion cells. APB (30-100 microM) reduced or blocked the light-evoked responses and resting firing rates of all ON-center ganglion cells; higher doses of APB (100 microM) were required to block the light-evoked responses of ON-transient cells. In contrast, an increase in resting firing rates was observed when L-APB was applied to some OFF-center ganglion cells. The EAA agonists kainate (KA) (10-20 microM) and NMDA (200-350 microM) increased the firing rate of virtually all ganglion cells examined. Quisqualate (10-20 microM) increased firing in most cells, but occasionally (4/13 cases) produced inhibition. The NMDA antagonist D-amino-phosphono-heptanoic acid (D-AP7) (200-250 microM) reduced the light-evoked responses of ganglion cells by an average of 12% from control levels, while resting firing rates declined 37%. In the presence of D-AP7, the basic receptive-field characteristics of cells were not significantly altered. In contrast, two non-NMDA receptor antagonists, NBQX (2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo-(F)-quinoxalinedione) and DNQX (6,7-dinitro-quinoxaline-2,3-dione), produced substantial reductions in the light-evoked responses (82%) and resting firing rates (87%) of all ganglion cell classes. A striking observation in some neurons was the recovery of a persistent transient light-evoked response in the presence of NBQX. This NBQX-insensitive, light-evoked response was always blocked by adding D-AP7. Thus, neurotransmission from bipolar to ganglion cells in primates is mediated predominantly by non-NMDA EAA receptors, with NMDA receptors forming a minor component of the light-evoked response.
authors.affiliation: Department of Physiology, University of Minnesota Medical School, Minneapolis.
authors.forename: E D
authors.initials: ED
authors.lastname: Cohen
authors.forename: R F
authors.initials: RF
authors.lastname: Miller
mesh_terms: D000613:Aminobutyrates / Q000494:pharmacology; D000818:Animals; D004594:Electrophysiology; D007395:Interneurons / Q000187:drug effects / Q000502:physiology; D008027:Light; D008252:Macaca fascicularis; D008253:Macaca mulatta; D016202:N-Methylaspartate / Q000494:pharmacology; D010215:Papio; D011810:Quinoxalines / Q000494:pharmacology; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors / Q000502:physiology; D017470:Receptors, Glutamate / Q000187:drug effects / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000502:physiology*
chemical_list: D000613:Aminobutyrates; D011810:Quinoxalines; D018091:Receptors, AMPA; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D016202:N-Methylaspartate; C012729:2-amino-4-phosphonobutyric acid