Iodide accumulates in milk at a concentration that is more than an order of
magnitude higher than the iodide concentration in maternal plasma. In earl
ier studies from our laboratory, we have shown that prolactin (PRL) enhance
s iodide accumulation by two- to threefold in cultured mammary tissues take
n from pregnant mice. In the present studies, we demonstrate via Western bl
otting techniques that prolactin elevates the quantity of the sodium iodide
symporter (NIS) in cultured mouse mammary tissues. In time-course studies,
the onset of the PRL effect of NIS accumulation was found to be between 4
and 16 h after addition of PRL to the explants. The lowest PRL concentratio
n that elicited a significant response was 1 ng/ml, and a maximum effect wa
s elicited with PRL concentrations >100 ng/ml. Actinomycin D, cycloheximide
, and thiocyanate abolished the PRL effect on NIS accumulation, whereas per
chlorate was without effect. These studies suggest that the PRL stimulation
of iodide accumulation in milk is mediated, at least in part, by the PRL s
timulation of NIS accumulation in mammary gland tissues. These studies furt
her demonstrate that the PRL effect on NIS accumulation occurs via an RNA p
rotein synthesis-dependent mechanism.