In the current study, treatment of animals with bromocriptine prevented the transient LH receptor mRNA peak between March 19 and 25 and reduced LH receptor mRNA levels below those of the pretreatment controls. This suggests a role for prolactin in regulation and maintenance of LH receptors. This hypothesis is indirectly supported by a number of studies showing that prolactin and/or placental lactogens increase LH receptor binding sites and LH receptor mRNA in the CL of other species. If present, the stimulatory effect of prolactin on mink LH receptors is transient, as it is not present during later gestation when prolactin levels are elevated and LH receptor mRNA remains constant.
Insufficient tissue was available for concurrent studies of LH binding. Nonetheless, other studies have shown that LH receptor mRNA abundance is highly correlated with LH binding to human and ovine ovarian tissues. The early peak in mink LH receptor mRNA is consistent with increases in the LH receptor in the feline CL associated with luteinization. Thereafter, similarities with known patterns of LH receptor or receptor mRNA are less evident. In general, LH receptor and/or its message increase with increased progesterone synthesis, while they remain constant during the midluteal phase in the mink. ampicillin antibiotic
In conclusion, fragments of the mink prolactin receptor and LH receptor genes were cloned and sequenced. The abundance of mRNA for both receptors varied significantly over the course of CL activation and early-postimplantation gestation. The pattern of expression for both of these genes was greatly influenced by reduction in endogenous prolactin levels, indicating that prolactin regulates its own receptor as well as influencing the LH receptor in the mink CL.