Characterization of the hepatic prolactin receptors induced by chronic iron deficiency and neuroleptics.

Nutritional iron deficiency (ID), like neuroleptic treatment, results in a reduction in dopaminergic activity and a rise in serum prolactin (PRL). Since PRL has been shown to regulate its own receptors, we studied PRL binding sites during the above treatments. ID induced in 21 day old male rats for 28 days, or treatment with either chlorpromazine (10 mg/kg per day i.p.) or fluphenazine (5 mg/kg per day i.p.) for 21 days or haloperidol (5 mg/kg per day i.p.) for 9 days, caused significant increases (3- to 8-fold) in [125I]oPRL specific binding to the liver membranes. The combined treatment with haloperidol and ID, as above, resulted in an additive effect on hepatic PRL receptors, suggesting that the actions of neuroleptics and ID may be either submaximal or mediated by two different mechanisms. After 7 days or recovery from ID, the induced PRL receptors were completely reduced to the control values. In vitro desaturation of the induced PRL binding sites with MgCl2 caused a further increase (1.57-fold) in PRL binding. Characterization of the hepatic PRL binding sites induced by ID showed properties similar to those reported for the classical PRL receptors, including specificity for the lactogenic hormones, a high affinity constant (2.38 X 10(10) M-1) and inhibition of PRL binding to the induced receptors by an anti-PRL receptor antibody. The results of this study further support the suggested role of endogenous PRL in inducing its own receptors.