Abstract 1. Retinal ganglion cell activity was recorded extracellularly in the intact cat eye. We examined the effects of iontophoretically applied glutamate (GLU), aspartate (ASP), and the specific agonists kainate (KA), quisqualate (QQ), (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), and N-methyl-D-aspartate (NMDA) on the spontaneous and light-driven activity of ganglion cells. 2. ASP and GLU increased the spontaneous as well as the light-driven activity of all brisk cell types. The effects of the two drugs were very similar. The activity of most cells remained at a constant increased level during prolonged application of these drugs. 3. KA also excited all brisk ganglion cell classes and caused effects very similar to those of GLU and ASP but was effective at a much lower concentration. In general, brisk ganglion cells responded most vigorously to KA application. 4. QQ excited approximately 50% of all ON-X and OFF-X cells encountered, the other 50% of the X cells and all Y cells were inhibited during QQ-application. This inhibition was quite likely due to the stimulation of glycinergic and GABAergic interneurons, because it was reduced or abolished during application of the respective antagonists strychnine and bicuculline. All ganglion cells apparently received either direct or indirect excitatory input from QQ receptors, which can be revealed by blocking the inhibitory interneurons. 5. The major actions of QQ on the discharge rate of ganglion cells are mimicked by AMPA. Hence, the actions of QQ are likely to be mediated by the "classical" QQ-receptor, ion-channel complex rather than by the recently described type of QQ-receptor that is coupled to a second messenger system. 6. NMDA excited ON-X, OFF-X, and OFF-Y cells but inhibited ON-Y cells. Excitatory and inhibitory NMDA effects could be blocked by the specific NMDA-receptor antagonists D(-)-2-amino-7-phosphono-heptanoate (AP-7) or 3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP). If the GABAergic transmission was blocked by bicuculline, the NMDA-induced inhibition of ON-Y cells was abolished. We conclude that NMDA activates GABAergic interneurons that in turn reduce the activity of ON-Y cells. Copyright © 1990 the American Physiological Society
Journal of Neurophysiology – The American Physiological Society
Published: Nov 1, 1990
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