Abstract
Haloperidol (30 nM, 3 μM) was found to increase prolactin release from GH4C 1 cells transfected with the D 2 receptor cDNA (GH4ZR 7) and from wild-type (untransfected) GH 3 cells, but not from wild-type GH4C 1 cells. In addition, haloperidol (3 μM) stimulated cAMP formation in GH 3 cells. It is suggested that haloperidol may act as an inverse agonist rather than as a neutral antagonist at dopaminergic D 2 receptors.