Defective dopaminergic regulation of prolactin secretion in a rat pituitary tumour cell line.

Abstract

IT is firmly established that certain rat1,2 and human3,4 pituitary tumours hypersecrete prolactin (PRL). Pituitary PRL secretion is probably under the dual control of hypothalamic prolactin-inhibiting and -releasing factors, and defective secretion in one or both of these factors could produce abnormal PRL secretion3. An alternative explanation for the in vivo PRL secretory defect of certain pituitary tumours is defective reception by the tumour of an appropriate hypothalamic endocrine signal. To test this latter hypothesis, we evaluated the effects of various catecholamines on PRL secretion in a cloned rat pituitary tumour cell line (GH3). Catecholamines are potent inhibitors of PRL secretion5, and it is postulated that the prolactin inhibiting factor may be a catecholamine6,7. We report here that dopamine failed to inhibit PRL secretion from the pituitary tumour cultures, whereas, other catechols added to our normal and pituitary tumour monolayer cultures suppressed prolactin release into the medium. In addition, apomorphine, which is postulated to be a specific dopaminergic agonist8–10, appropriately suppressed PRL secretion in the tumour monolayer cultures. Our results therefore provide evidence for an unusual dopaminergic defect in the GH3 rat pituitary tumour cell line.