Haloperidol-induced increases in rat amygdaloid dopamine metabolism: evidence for independence from postsynaptic feedback mechanisms.

The present study assessed the role of postsynaptic dopamine (DA) receptors in mediating the actions of focal injections of the classical antipsychotic drug, haloperidol, on DA metabolism in the rat amygdala (AMYG) and caudate-putamen (CP) using a high-performance liquid chromatographic assay. One hour after unilateral injection of haloperidol into either site, significant elevations of the DA metabolite, homovanillic acid, were observed in both ipsilateral (+33%) and contralateral (+81%) hemispheres of the CP and in the ipsilateral (+107%) and contralateral AMYG (+121%). Such increased DA metabolism persisted in these regions if focal injections of muscimol (intended to eliminate transmission in postsynaptic output neurones) had been made into either brain area immediately prior to the focal haloperidol injection. It is argued that neurones lying postsynaptic to DA terminals in both the AMYG and CP are unnecessary for the ability of haloperidol to increase DA metabolism in these regions.