The termination of delayed implantation in the fur seal (Daniel, 1971,1974), mouse (Aitken, 1977), rat (Surani, 1975) and roe deer (Aitken, 1974,1975) is thought to be associated with the oestrogen-induced release of a protein-rich endometrial secretion into the uterine lumen. Finn (1974), however, observed that the intraperitoneal injection of actinomycin D, an inhibitor of protein synthesis, terminated delayed implantation in the mouse within 48–72 h. It was suggested that actinomycin D released the blastocysts from their state of diapause by inhibiting the transcription of a proteinaceous inhibitor of blastocyst attachment (Finn, 1974). Actinomycin D may, however, have increased the protein content of the uterine lumen either through the 'superinduction' of uterine proteins (Tomkins et al., 1969) or, possibly, through the stress-induced release of steroids from the adrenal glands. A study was therefore designed to determine the influence of actinomycin D on uterine secretory activity in the mouse.
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