Striatal neurochemistry and motor activity were assessed in cats treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and killed either when symptomatic for a Parkinson-like motor disorder or six weeks later, when showing significant motor recovery. The results of striatal neurochemical analyses showed distinct regional differences in susceptibility to MPTP-induced damage, with dorsal striatal regions generally more severely affected than ventral striatal regions. Symptomatic animals had more severe dopamine loss in all striatal regions than did recovered animals. The dorsal lateral caudate, the cat's sensorimotor striatum, had the largest dopamine depletion in the symptomatic animals (99%) and the least recovery in recovered animals (94% depletion). In contrast, the nucleus accumbens had a 94% dopamine depletion in symptomatic animals and only a 34% depletion in recovered animals. In addition to increases in dopamine levels and dopamine utilization in the striatum in recovered animals, significant increases in serotonin levels and serotonin utilization were also observed. Therefore, motor recovery may have been due to either or both of these neurochemical changes. The fact that the cat develops Parkinson-like motor symptoms but that they are not persistent may make this an interesting model in which to study the role of dopamine in motor function and to study compensatory mechanisms of the damaged dopamine system.