The ranch mink was studied to determine the role of pituitary luteotro
phins on corpus luteum (CL) function before and after implantation. Tw
elve mink were treated with monoclonal antiserum against gonadotrophin
-releasing hormone (GnRH), and 12 with an irrelevant monoclonal antibo
dy during embryonic diapause. Activation of the CL, plasma progesteron
e concentration and embryo implantation were unaffected by this treatm
ent. In a second trial, groups of ten mink were treated with GnRH anti
bodies, 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 compromis
ed postimplantation CL function by inducing regression of the corpus l
uteum. Incubation of dissociated luteal cells from ovaries of mink at
21-24 days after implantation with either LH or prolactin increased th
e accumulation of progesterone over 2 h. Addition of 25-hydroxy-choles
terol (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 intera
ction between prolactin and canine low-density lipoproteins (LDL) in t
he stimulation of progesterone secretion in vitro. The results are int
erpreted to indicate that LH/FSH are not required for luteal support d
uring embryonic diapause, or for luteal activation. Prolactin is neces
sary for luteal activation, and LH and/or FSH and prolactin are obliga
te luteotrophins during the postimplantation period in the mink.