Abstract
When toad retinae were incubated with veratrine, kainic acid and L-.alpha.-amino adipic acid, photoreceptor cells survived and most other neurons died. This preparation of isolated photoreceptor cells accumulated radioactive molecules from the incubation medium and metabolized these into labeled compounds. When a preparation was placed on a filter and superfused, radioactive molecules which were released into the superfusion fluid could be collected and later analyzed. Several procedures was used for inducing the release of possible transmitter compounds. Each released compound was chemically identified. Three compounds, aspartic acid, glutamic acid and N-acetyl histidine, were released when the K concentration was increased in media that lacked Ca and contained cobalt. The release of these compounds was further increased when Co was removed and Ca returned to the extracellular medium. Two additional compounds, putrescine and cadavarine, were also released during depolarization when Ca was present. The efflux of compounds was also increased by homo- and hetero-exchange. For at least aspartate, exchange was Na-dependent. The post-synaptic effect of released compounds was tested by their ability to increase the efflux of [3H]GABA from isolated horizontal cells. Doses of 0.1 mM L-aspartate or L-glutamate produced an increase in GABA efflux. N-acetyl histidine, putrescine and cadavarine were ineffective. Isolated photoreceptors and intact retinae were incubated with [3H]aspartate or [3H]putrescine. Subsequent histology and autoradiography demonstrated that both compounds were selectively accumulated by cones.