Kainic acid (KA), an extended analog of L-glutamate, was injected into the eyes of living goldfish. After survival times ranging from 15 min to 6 days, retinae were inspected for KA-induced degeneration at both the LM and EM levels. KA had little effect on photoreceptors, mixed rod-cone bipolar cells, Mu¨ller cells, at least two types of amacrine cells and the optic nerve. Reversible edema was seen in both rod and cone horizontal cells. Pure cone bipolar cells and the majority of amacrine cells appeared to be destroyed by KA. The effect of KA is selective not only on the cell types involved, but also in the location of KA-induced edema on the affected cells, i.e., soma and proximal portions of dendrites of cone horizontal cells as opposed to the distal ends of dendrites of rod horizontal cells. Implications of these data are discussed in regard to the use of KA as a probe for glutamatergic pathways in the retina. One hypothesis suggested by our results is that rods use glutamate whereas cones use aspartate as their neurotransmitter.