Destruction of norepinephrine terminals in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice reduces locomotor activity induced by L-dopa.

There is little information concerning the effects of norepinephrine (NE) depletion on clinical features of patients with Parkinson's disease. By inducing two types of experimental parkinsonism, one with a dopamine (DA) deficiency alone and the other with both a DA and NE deficiency, we attempted to evaluate the differences in locomotor activity and behavioral responses between the two groups after L-DOPA administration. The results of the study revealed that increases in locomotor activity were markedly suppressed in the DA and NE deficient group. This may suggest that with striatal DA deficiency the central NE terminals play a significant role in the increase in locomotor activity after L-DOPA administration.