Single, monolateral injection into rat substantia nigra of
manganese chloride produced within two weeks from its administration a loss of
dopamine in the striatum ipsilateral to the injected side. The effect was dose-dependent and was not extended to serotoninergic terminals present in this brain area, whose content in
serotonin and 5-hydroxyindoleacetic
acid was not affected. When
L-DOPA +
carbidopa or
pargyline were given to these animals the decrease of striatal
dopamine was more marked. Moreover, rats treated two weeks before with a dose of
manganese chloride that produced a 70-80% drop in striatal
dopamine concentrations, rotated ipsilaterally to the
dopamine-depleted striatum when injected with
apomorphine, suggesting that in these animals the stimulatory effects of
apomorphine were more relevant in striatum where presynaptic dopaminergic neurons were not affected by
manganese chloride. These data indicate that the alterations of dopaminergic postsynaptic receptors may be different in parkinsonian and in
manganese-intoxicated patients and that current
therapy used for
Parkinson's disease could be a hazard in treating
manganese poisoning.