THE ROLE OF NMDA AND NON-NMDA EXCITATORY AMINO-ACID RECEPTORS IN THE FUNCTIONAL-ORGANIZATION OF PRIMATE RETINAL GANGLION-CELLS

The role of excitatory amino acid (EAA) receptors in primate retinal g anglion cell function was analyzed in a superfused retina-eyecup prepa ration using single-unit, extracellular recording techniques. The effe cts of bath applied L-2-amino-4-phosphonobutyrate (APB), N-methyl-D-as partate (NMDA), and non-NMDA EAA receptor agonists and antagonists wer e examined on the light-evoked responses and resting firing rates of g anglion cells. APB (30-100 mu M) reduced or blocked the light-evoked r esponses and resting firing rates of all ON-center ganglion cells; hig her doses of APB (100 mu M) were required to block the light-evoked re sponses of ON-transient cells. In contrast, an increase in resting fir ing rates was observed when L-APB was applied to some OFF-center gangl ion cells. The EAA agonists kainate (KA) (10-20 mu M) and NMDA (200-35 0 mu M) increased the firing rate of virtually all ganglion cells exam ined. Quisqualate (10-20 mu M) increased firing in most cells, but occ asionally (4/13 cases) produced inhibition. The NMDA antagonist D-amin o-phosphono-heptanoic acid (D-AP7) (200-250 mu M) reduced the light-ev oked responses of ganglion cells by an average of 12% from control lev els, while resting firing rates declined 37%. In the presence of D-AP7 , the basic receptive-field characteristics of cells were not signific antly altered. In contrast, two non-NMDA receptor antagonists, NBQX (2 ,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo and DNQX (6,7-dinitro-quinoxali ne-2,3-dione), produced substantial reductions in the light-evoked res ponses (82%) and resting firing rates (87%) of all ganglion cell class es. A striking observation in some neurons was the recovery of a persi stent transient light-evoked response in the presence of NBQX. This NB QX-insensitive, light-evoked response was always blocked by adding D-A P7. Thus, neurotransmission from bipolar to ganglion cells in primates is mediated predominantly by non-NMDA EAA receptors, with NMDA recept ors forming a minor component of the light-evoked response.