Excessive aluminum exposure and accumulation has been implicated as the cause of two disorders which display learning deficits (dialysis encephalopathy and Alzheimer's disease). To develop an animal model, rabbits were given 20 sc Al lactate injections (0, 25, 50, 100, 200 or 400 mumole/kg) over 4 weeks. Dose dependent weight reductions were observed. Two weeks later the baseline frequency of nictitating membrane extension (NME) was determined. Differential classical conditioning of the NME was then conducted. No treatment group differences were observed in frequency of baseline NME, amplitude of the response to shock, or shock threshold to produce NME, suggesting no aluminum effects on the subjects' ability to perform the response. All subjects developed the discrimination. The 200 and 400 group acquired the conditioned response less well than controls, as shown by a lower percent of conditioned responses in the second half of the conditioning sessions (80 and 74% of controls) and a greater latency to onset of the conditioned response (327 and 310 msec vs. 261 msec for controls). These results indicate that chronic systemic exposure of adult rabbits to 1 results in learning deficits not due to sensory or motor impairment of the learned response.