Dopamine D1 receptor analogues act centrally to stimulate prolactin secretion in ewes

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Abstract
It is well known that prolactin secretion is inhibited by dopamine acting via the pituitary dopamine D2 receptor. Dopamine D1 receptor analogues also affect prolactin levels although the mechanisms and physiological significance are poorly understood. The present study of the ewe was undertaken to characterize the effects of the D1 receptor agonist SKF 38393 and antagonist SCH 23390 on prolactin in this species and to determine whether the prolactin response to both drugs requires an intact hypothalamo-pituitary axis. Ovariectomized ewes were injected intravenously with vehicle, 0·2, 2 or 20 mg SKF 38393 (D1 agonist) or SCH 23390 (D1 antagonist). At the 20 mg dose, plasma prolactin concentrations were significantly (P P 1 agonist stimulated prolactin secretion via a direct effect on central dopamine D1 receptors whereas the D1 antagonist interacted with the pituitary dopamine D2 receptor to increase prolactin secretion. In a further experiment this hypothesis was tested in hypothalamo-pituitary disconnected ewes which were infused with dopamine (0·5 μg/kg per min) for 3 h. After 2 h of the dopamine infusion, animals were challenged with intravenous injections of the vehicle, 20 mg SKF 38393, 20 mg SCH 23390 or 2 mg domperidone (dopamine D2 antagonist). Infusion of dopamine was followed by a significant (P P 1 agonist SKF 38393 or antagonist SCH 23390 increase prolactin secretion in the ewe. The prolactin response to either drug requires an intact hypothalamo-pituitary axis indicating that SKF 38393 and SCH 23390 act at some central site(s) which is linked with hypothalamic secretion of prolactin-releasing or -inhibiting factors. Journal of Endocrinology (1993) 137, 457–464

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