Control of luteal function in the mink (Mustela vison).

The ranch mink was studied to determine the role of pituitary luteotrophins on corpus luteum (CL) function before and after implantation. Twelve mink were treated with monoclonal antiserum against gonadotrophin-releasing hormone (GnRH), and 12 with an irrelevant monoclonal antibody during embryonic diapause. Activation of the CL, plasma progesterone concentration and embryo implantation were unaffected by this treatment. In a second trial, groups of ten mink were treated with GnRH antibodies, bromocriptine, bromocriptine plus 0.5 mg prolactin per day per animal, or ethanol vehicle. Comparison of the consequent profiles of progesterone indicated that both bromocriptine and anti-GnRH compromised postimplantation CL function by inducing regression of the corpus luteum. Incubation of dissociated luteal cells from ovaries of mink at 21-24 days after implantation with either LH or prolactin increased the accumulation of progesterone over 2 h. Addition of 25-hydroxy-cholesterol (25OHC) as substrate increased basal levels and the progesterone accumulation stimulated by LH and prolactin; the increases induced by luteotrophins were additive. There was an apparent synergistic interaction between prolactin and canine low-density lipoproteins (LDL) in the stimulation of progesterone secretion in vitro. The results are interpreted to indicate that LH/FSH are not required for luteal support during embryonic diapause, or for luteal activation. Prolactin is necessary for luteal activation, and LH and/or FSH and prolactin are obligate luteotrophins during the postimplantation period in the mink.