Effect of selective kainate lesions on the release of glutamate and aspartate from chick retina

In order to contribute evidence leading to establishing the excitatory pathways in the vertebrate retina, we selectively lesioned chick retinas by intraocular injection of 6, 60, 120, and 200 nmol of kainate, which selectively damages OFF‐bipolars, amacrines, horizontals, and ON‐bipolars, and measured the K+‐stimulated, Ca++‐dependent release of L‐(3H)‐glutamate and L‐(3H)‐aspartate. We also measured (3H)‐GABA release as a marker for horizontal cells and a population of amacrines, as well as (14C)‐glycine release as a tracer of a different subpopulation of amacrines. All four amino acids were released from control retinas by a depolarizing K+ concentration in a Ca++‐dependent fashion. GABA and glycine, however, showed an additional Ca++‐independent component of release. Lesion induced by 6 nmol of kainate decreased by 50% the release of glutamate and by 20% that of aspartate; glycine release was reduced 40% while GABA release was unaffected. Injection of 60 nmol of kainate reduced glutamate release a further 20% and significantly decreased GABA (50%) and glycine (75%) release; aspartate release remained unmodified; 120 nmol of kainate caused a further 30% reduction in aspartate and GABA release. Neither compound was significantly released after treatment with 200 nmol of kainate. These results seem to suggest that while OFF‐bipolars could release glutamate as transmitter, aspartate is released from a different cell population which is less sensitive to kainate, probably ON‐bipolars.