Effects of remoxipride and raclopride on prolactin release from clonal pituitary tumour cells.

The dopamine D2 receptor antagonist remoxipride (30 microM) stimulated prolactin release from the prolactin-producing rat pituitary tumour cell strains GH3 and GH4C1 as well as from transfected GH4C1 cells expressing the short isoform of the rat D2 receptor (GH4ZR7). The effect of remoxipride on prolactin release is probably not due to an interaction with D2 receptors since GH4C1 cells, in contrast to GH3 and GH4ZR7 cells, are completely devoid of D2 receptors; in contrast, we have previously shown that the D2 antagonist haloperidol causes prolactin release from D2 receptor-expressing cells, only. Exposure of GH3 cells to the inhibitor of intracellular Ca2+ mobilization, 8-(diethylamino)-octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8) prevented the prolactin-releasing effect of remoxipride whereas pretreatment with the membrane Ca2+ channel antagonist nimodipine did not influence the response. The D2 receptor antagonist raclopride counteracted the reduction of VIP-stimulated prolactin release induced by the D2 agonist quinpirole but caused no prolactin release per se.