Acute recruitment of prolactin-secreting cells is regulated posttranscriptionally.

17 beta-estradiol (E2) stimulates the release of an activity from neurointermediate lobe (NIL) cells which increases the relative abundance of prolactin (PRL) secretors in cultures of anterior pituitary (AP) cells. In the present study, we sought to determine whether this NIL/E2 effect was due to recruitment of growth hormone (GH)-releasing cells into the PRL-secreting population and to define the mechanism regulating this induction of PRL secretors. AP cells from ovariectomized rats were cultured overnight, exposed to NIL/E2 treatment (or medium alone) for 3 h and then subjected to reverse hemolytic plaque assays for PRL and GH release. We found that exposure to NIL/E2 increased by 10% the proportion of AP cells that secreted PRL but did not influence the overall abundance of cells that released GH. A more critical analysis of these cultures revealed that all of the newly recruited PRL-secreting cells also released GH. This increment in the proportion of cells that released both PRL and GH concurrently was accompanied by an equivalent decrease in the fraction that secreted GH alone. Thus, it appeared that NIL/E2 treatment initiated PRL secretion by cells that previously released only GH. We then tested whether this induction of PRL secretors required the synthesis of proteins and/or RNA. We found that the protein synthesis inhibitor cycloheximide completely abolished the recruitment of PRL-releasing cells by NIL/E2 treatment, whereas the RNA synthesis inhibitor actinomycin D had no effect on this response. We conclude that NIL/E2 treatment induces PRL secretion by cells that formerly released only GH and that this induction is regulated posttranscriptionally.