Glutamate, when puffed near the synaptic terminals, elicits a current in rod photoreceptors. The current is strongly dependent upon both the intracellular and extracellular chloride concentration: its reversal potential follows the predicted Nernst potential for a chloride permeable channel. The glutamate-elicited current also requires the presence of extracellular sodium. This glutamate-elicited current is pharmacologically like a glutamate transporter: it is elicited, in order of efficacy, by L-glutamate, L-aspartate, L-cysteate, D-aspartate, and D-glutamate, all shown to activate glutamate transport in other systems. Furthermore, it is reduced by the glutamate transport antagonists dihydrokainate (DHKA) and D,L-threo-3-hydroxyaspartate (THA). THA, when applied alone, elicits a current similar to that elicited by glutamate. The current cannot be activated by the glutamate receptor agonists kainate, quisqualate, NMDA and APB, nor can it be blocked by the glutamate receptor antagonists CNQX and APV. Thus, the current does not appear to be mediated by a conventional glutamate receptor. Taken together, the ionic dependence and pharmacology of this current suggest that it is generated by glutamate transporter coupled to a chloride channel.