It is well known that neuroleptic-induced catalepsy in rats intensifies upon repeated testing. Here, the question is addressed whether intensification of catalepsy results from intermittent drug administration or from intermittent context exposure. In experiment 1, rats were treated with intermittent haloperidol injections (0.25 mg/kg) followed by the catalepsy test (descent latency from the horizontal bar). In experiment 2, rats were lesioned with 6-hydroxydopamine injections into the striatum, resulting in a 45% reduction of dopamine concentration. Catalepsy was tested intermittently for several weeks. In both experiments we found a very stable intensification of catalepsy over 9 (haloperidol rats) and 11 (lesioned rats) days, showing that intensification is not due to intermittent dopamine depletion. In both experiments, intensification of catalepsy was very stable and was observed 18 days later in haloperidol-treated rats and 101 days later in lesioned animals. However, a change of the environmental context abolished the intensified catalepsy in both experiments. It is concluded that intensification of catalepsy is due to intermittent context exposure rather than intermittent drug administration. It is generally accepted that 6-hydroxydopamine lesions represent an animal model of Parkinson's disease. Given the results above, context-dependent intensification of parkinsonian symptoms might also occur in Parkinson's disease, and its prevention should be taken into consideration for future therapy of the disease.