Prolactin antagonizes the corticoid-promoted development of adult-type epidermis in cultured larval bullfrog skin.

EDTA-treated larval bullfrog skin, in which apical and skein cells had been removed and only basal cells remained, was cultured in one of four media. These contained either aldosterone (Aldo) or a mixture of Aldo, hydrocortisone (HC) and corticosterone (C), each either supplemented with prolactin (PRL) or lacking PRL. Skin cultured with Aldo alone or with the corticoid mixture (Aldo + HC + C) developed an adult-type epidermis: (i) both types of skin reacted to human blood group antigen A, a marker for the adult-type epidermis of bullfrog skin; (ii) amiloride decreased the short-circuit current Isc in these skin preparations, but acetylcholine (ACh) had no effect on the Isc. It seemed to make little difference to the results whether the skin was cultured with Aldo or with the corticoid mixture. PRL antagonized the action of Aldo and induced the development of a larval-type epidermis in both skin preparations: (i) the skin preparations did not react to human blood group antigen A; (ii) acetylcholine and amiloride each stimulated Isc in these preparations. Since ACh and amiloride each stimulated the Isc in skin with apical cells, ACh/amiloride-stimulated channels may be located on these cells.