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However, many pharmacological studies have suggested an autoreceptor role for the DA D<jats:sub>3<\/jats:sub>receptor. This possibility was tested with mice lacking the D<jats:sub>3<\/jats:sub>receptor as a result of gene targeting. The basal firing rates of DA neurons within both the substantia nigra and ventral tegmental area were not different in D<jats:sub>3<\/jats:sub>receptor mutant and wild-type mice. The putative D<jats:sub>3<\/jats:sub>receptor-selective agonist<jats:italic>R<\/jats:italic>(+)-<jats:italic>trans<\/jats:italic>-3,4,4<jats:italic>a<\/jats:italic>,10<jats:italic>b<\/jats:italic>-tetrahydro-4-propyl-2<jats:italic>H<\/jats:italic>,5<jats:italic>H<\/jats:italic>-(1)benzopyrano(4,3-<jats:italic>b<\/jats:italic>)\u22121,4-oxazin-9-ol (PD 128907) was equipotent at inhibiting the activity of both populations of midbrain DA neurons in the two groups of mice. In the \u03b3-butyrolactone (GBL) model of DA autoreceptor function, mutant and wild-type mice were identical with respect to striatal DA synthesis and its suppression by PD 128907.<jats:italic>In vivo<\/jats:italic>microdialysis studies of DA release in ventral striatum revealed higher basal levels of extracellular DA in mutant mice but similar inhibitory effects of PD 128907 in mutant and wild-type mice. These results suggest that the effects of PD 128907 on dopamine cell function reflect stimulation of D<jats:sub>2<\/jats:sub>as opposed to D<jats:sub>3<\/jats:sub>receptors. 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