Blastocyst’s State of Activity and the Window of Implantation in the Mouse

Abstract

Synchronized development of the embryo to the blastocyst stage and differentiation of the uterus to the receptive state are critical to the process of implantation (1). The attainment of a differentiated uterus to support embryo development and implantation is primarily the result of the coordinated effects of estrogen and progesterone (P₄) (1, 2). In rodents the first conspicuous sign that the implantation process has been initiated is an increased endometrial vascular permeability at the site of the blastocyst apposition. This can be visualized as discrete blue bands along the uterus after an intravenous (IV) injection of a macromolecular blue dye solution (1). This increased vascular permeability coincides with the initial attachment reaction between the trophectoderm and uterine luminal epithelium (ULE) (3). The permeability reaction is considered one of the earliest prerequisite events in the implantation process (1). In the mouse the attachment reaction occurs at 2200–2300 h on day 4 of pregnancy and is preceded by luminal closure that results in an intimate apposition of the blastocyst to the ULE (1, 3, 4). The attachment reaction is followed by stromal decidualization and ULE apoptosis at the site of blastocyst (3, 5). This results in the subsequent adherence and penetration by trophoblasts through the underlying basement membrane (6). Trophoblast invasion continues through the stroma in a regulated manner by the remodeling of the extracellular matrix (ECM).