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S. R. Milligan, A. A. Khan, and B. C. Thorne

Summary. Treatment of female mice with bromocriptine on Day 1 or 3 of pregnancy induced many of the females to return to oestrus. The incidence of extended cycles (7–10 days) and pseudopregnancies following this return to oestrus was significantly higher than in unmated control females. These observations are consistent with the existence of a 'mnemonic' component of the luteotrophic system in the mouse.

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S. R. Milligan, H. M. Charlton, and E. Versi

Summary. The development of luteal function in the vole is dependent on a neuroendocrine reflex which is initially activated by mating. Bromocriptine was used to destroy the CL initially induced by mating and fresh CL were induced by hormone treatment. The fate of such newly formed CL suggested that the luteotrophic effect of mating continued for about 10 days after mating, despite the destruction of the original mating-induced CL. The luteotrophic effect of mating therefore seems to be 'remembered'. A study of the fate of hormonally induced CL in females in which pregnancy had been blocked by exposure to a strange male suggested that the strange male may cause pregnancy failure by inhibiting or suppressing the luteotrophic 'mnemonic' activated by the stud mating.

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H. M. Charlton, S. R. Milligan, and E. Versi

Summary. The lifespan of corpora lutea resulting from hormonally induced ovulations was prolonged by exogenous prolactin, concurrent lactation, or pregnancy. Treatment of mated females with bromocriptine resulted in failure of luteal function only when the drug was given before Day 6 of pregnancy. Pregnancy was dependent on the presence of the ovaries in its later stages. The results suggest that prolactin is luteotrophic in early pregnancy but that a placental luteotrophin may become effective by Day 6 of pregnancy.

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C. A. Finn, M. D. Pope, and S. R. Milligan

Summary. Oil, carrageenan or saline were injected into the uteri of ovariectomized mice treated with hormones on schedules which would sensitize, partly sensitize or not sensitize the uterus to an intraluminal decidual stimulus. The uterine epithelium was examined histologically at various times over the succeeding 5 h. Saline did not produce any morphological change whereas almost immediately after the injection of oil or carrageenan epithelial cell death was apparent in the uterus, regardless of hormone treatment. Within 45 min the dead cells had been removed and the epithelium was re-established. Oil droplets were still present in the uterus after 5 h and these were able to stimulate a decidual reaction in partly sensitized animals when oestrogen was administered 18–44 h after the oil instillation, well after the re-establishment of the epithelium. It is suggested that the early transient cell death in the uterine epithelium is not responsible for triggering the decidual reaction but that it is the contact of the oil droplet with an intact epithelium which triggers the response when the hormonal conditions so allow.

Keywords: decidualization; uterus; implantation; endometrium; mouse