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Biology of Reproduction, Vol 25, 487-491, Copyright © 1981 by Society for the Study of Reproduction
1 Department of Physiology,
New York State College of Veterinary Medicine,
Cornell University The purpose of this experiment was to determine whether prolactin (PRL) is the factor that
activates the quiescent corpus luteum (CL) and terminates the delay that precedes implantation in
mink. Animals were hypophysectomized or sham-hypophysectomized 6 days after the second of
two matings. Eight hypophysectomized mink received 0.5 mg ovine PRL (NIH-P-S13) daily
through Days 21-24 of the experiment (Day 0 = day of surgery). Five sham-hypophysectomized
and one hypophysectomized animal received no hormone therapy after surgery. All animals were
bled at 3 day intervals until termination by exsanguination between Days 21 and 24. Uteri were
observed by means of midventral laparotomy between Days 14 and 16. The hypophysectomized, untreated mink displayed neither luteal activation nor embryo implantation throughout the duration of the experiment. In hypophysectomized mink injected with
PRL, luteal activation, as indicated by an increase in peripheral progesterone above pretreatment
levels, had begun by Day 3 and persisted through Day 15 (P<0.05). Uterine swellings were present
in six of eight PRL-treated mink at Days 14-16 and in seven of eight at Days 21-24. These
swellings were found to contain implanted embryos at necropsy. Luteal activation occurred by Day
9 in sham-hypophysectomized mink, and progesterone continued to increase through Day 24. No
evidence of implantation was present at Days 14-16 in this group but three of five had implanted
by Days 21-24. The results demonstrate that PRL alone will induce luteal activation and embryo implantation
in hypophysectomized mink. However, PRL alone appeared not to be able to sustain luteal function. It is suggested that photoperiod acts through hypophyseal PRL secretion to terminate embryonic diapause in mink.
2 USDA Fur and Sheep Research Station, SEA,
Cornell University,
Ithaca, New York 14854
Note:
ACKNOWLEDGMENTS
This study was supported by the U. S. Mink Farmers Research Foundation Grant to P. W. Concannon
and National Research Council of Canada Grant
A9743 to B. D. Murphy. We thank W. Gardner for aid
in breeding animals; S. Guisti, B. Hodgsen, and J.
Deiden for technical assistance; and Drs. W. R. Butler
and G. D. Niswender for contribution of antiserum.
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