The hyperkinetic syndrome following long-term haloperidol treatment: Involvement of dopamine and noradrenaline

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Abstract
Mice withdrawn for 7 days from a 35-day treatment period with haloperidol (3 mg/kg/day) displayed significantly greater spontaneous locomotor activity (hyperkinesia) than animals withdrawn from the vehicle. The hyperkinesia was antagonized by phenoxybenzamine (anα-adrenergic receptor antagonist) and by FLA-63 (a dopamine-β-hydroxylase inhibitor) but not by haloperidol (a dopamine receptor antagonist).α-Methyl tyrosine (a tyrosine hydroxylase inhibitor) was effective in antagonizing the hyperkinesia and this blockade byα-methyl tyrosine could be completely reversed by the administration of a low dose of the catecholamine precursor, DOPA. The data suggest that noradrenergic systems are of importance for the manifestation of the hyperkinetic syndrome seen in mice withdrawn from long-term haloperidol treatment.