The effect of haloperidol and apomorphine, and both drugs in combination, on the 
first steps in the synthesis of catecholamines and 5-hydroxytryptamine (5-HT) 
has been studied in three rat brain regions. The rate of formation of dopa and 
5-hydroxytryptophan (5-HTP) was studied by measuring the accumulation of these 
amino acids during 30 min after administration of the inhibitor of the aromatic 
L-amino acid decarboxylase, NSD 1015 (3-hydroxybenzylhydrazine HCl). Haloperidol 
caused an increase in dopa and no change in 5-HTP formation. The threshold dose 
was severalfold higher in the noradrenaline-predominated hemisphere portion than 
in the dopamine-rich striatal and limbic regions, suggesting a higher affinity 
of haloperidol for dopamine than for noradrenaline receptors. Apomorphine caused 
a decrease in dopa formation in all three brain regions studied, although the 
effect was much more pronounced in the regions dominated by dopamine. The 
threshold dose was about 30 microng/kg, i.e. an order of magnitude lower than 
the threshold dose for apparent postsynaptic dopaminergic receptor activation. 
This discrepancy is suggested to be due to preferential activation of inhibitory 
dopaminergic autoreceptors by low apomorphine doses. This phenomenon may also 
contribute to explain the complex dose-response curves of apomorphine. Low doses 
of apomorphine caused a decrease and high doses an increase in 5-HTP formation. 
These effects, like those on noradrenaline synthesis, are suggested to be 
secondary to activation of dopaminergic pre- and post-synaptic receptors. The 
interaction between apomorphine and haloperidol with respect to dopa formation 
appears to be largely explicable on the assumption of a competition between an 
agonist and an antagonist for dopaminergic receptors. However, very large doses 
of apomorphine cause a haloperidol-resistant inhibition of tyrosine, and 
probably also tryptophan, hydroxylation, which may be due to a direct inhibition 
of the aromatic amino acid hydroxylase involved.