Axoplasmic transport along the optic axons was studied after intraocular injections of kainic acid (KA). Transport of labeled material did not initiate from the eye when KA was injected simultaneously with the protein precursor [3H]proline. When KA was injected after axoplasmic transport of labeled proteins had begun, no additional radioactive material moved out of the retinal ganglion cells. However, the labeled material already present in the optic nerve at the time of KA injection continued to move, and accumulated at the nerve endings. Although KA reduces the incorporation of precursor, this effect of KA on axoplasmic transport appears to be more than a consequence of inhibition on precursor uptake or protein synthesis. Recovery from this KA action began 6 h after exposure to KA and was about 50% recovered by 36 h. The extent of the recovery remained at this level for as long as a week, which suggested a partial recovery of the ganglion cells. A second exposure to KA after the inner plexiform layer had virtually disappeared was as effective as the first exposure in preventing the appearance of transported protein in the optic nerve, suggesting a direct action of KA on the ganglion cells. We interpreted the results to indicate that KA interferes with the initiation phase of axoplasmic transport in ganglion cells and this effect is partially reversible.