Depletion of monoamine transmitters by tetrabenazine in brain tissue in Huntington's disease.

The neurochemical effect of tetrabenazine was assessed by determining the levels of dopamine, noradrenaline and 5-hydroxytryptamine and their metabolites in post-mortem brain from Huntington's disease patients with or without a history of tetrabenazine treatment. The tetrabenazine-treated group showed a general description of monoamines in all regions studied, the greatest reduction being dopamine in the caudate. This provides the basis for the effect of tetrabenzine on chorea, while monoamine losses in limbic regions may mediate the production of side effects, such as depression.