Effects of Cholera and Pertussis Toxins on Prolactin Stimulation of Lactose Synthesis and Ornithine Decarboxylase Activity in Mouse Mammary Gland Explants

Abstract

Summary

Abstract. Studies indicate that G proteins are likely involved in the signal transduction pathway for prolactin's stimulation of mitogenesis in Nb₂ cells. In the mammary gland, little is known about the possible role of G proteins in the prolactin (PRL) stimulation of milk product synthesis. Therefore, the effects of cholera and pertussis toxin, enzymes that modify G protein activity, were tested on several actions of prolactin on mouse mammary tissue in culture. At concentrations of 0.1-0.5 μg/ml, cholera toxin stimulated ornithine decarboxylase activity in a dose-response fashion; when tested in concert, cholera toxin and prolactin caused an additive response. Cholera toxin by itself did not affect the rate of lactose synthesis, but at concentrations above 0.5 μg/ml, it attenuated the magnitude of the prolactin stimulation of lactose synthesis. Pertussis toxin (0-0.5 μg/ml), both by itself and in concert with PRL, had no effect on ornithine decarboxylase activity. At concentrations of 25 ng/ml and above, pertussis toxin inhibited the PRL stimulation of lactose synthesis, whereas at 0.2 and 0.5 μg/ml, pertussis toxin abolished the PRL response. These observations suggest that a G protein, but not G_s, may be involved in prolactin's mechanism of signal transduction in the mouse mammary gland.