It was reported that that there was a fast action of estrogen on the target cells. Recent researches on some kinds of cells have suggested that G protein-coupled receptor 30 (GPR30) is involved in the rapid effects of estrogen as its membrane receptor. The aim of this research is to reveal whether GPR30 mediates the fast action of estrogen on mouse blastocyst and its role in embryo implantation. We firstly used RT-PCR to detect the expression of GPR30 mRNA, immunocytochemistry to detect the expression of GPR30 protein and FITC- E2-BSA to detect the binding sites of estrogen in the mouse blastocyst cells further to be compared with the GPR30’s location. We found that the mRNAs and proteins expressed on the mouse blastocyst cells and their location was mostly consistent with the binding sites of estrogen on the plasma membrane (Figure 1). To study GPR30 mediating the fast action of estrogen on mouse blastocyst, we used Fluo-3/AM (3μmol/L) to label intracellular calcium and confocal laser scanning microscopy to detect the dynamic change of [Ca2+]i in different groups of mouse blastocysts, which were treated respectively with 1μmol/L E2, 1μmol/L E2-BSA, 1μmol/L G1, a GPR30-specific agonist and 1μmol/L G15, a GPR30-specific antagonist, followed by 1μmol/L E2-BSA. The results showed that E2, E2-BSA as well as G1 could induce their rapid increase of Cai2+ , while G15 could inhibit the fast effect of E2-BSA (Figure 2). To study the role of GPR30 mediating the effect of estrogen on mouse blastocyst in implantation, total 53 blastocysts from donor mice were divided into two groups, one is G15 group (n=26) in which blastocysts were pretreated with 1μmol/L G15 for 30 minutes, the other one is for control (n=27) in which blastocysts were pretreated with the same amount of vehicle, and then both groups of blastocysts were separately transplanted into the bilateral uterine horns of five day 4 pseudopregnant recipient mice and the implantation rates on day 10 between two groups were compared. The results indicated that the implantation rate of G15 group was 19.2%, significantly lower than 55.5% of control group (P<0.05). Recent studies have implicated GPR30 as a mediator of the rapid effects of estrogens in some kinds of cells. We provided the first evidence that GPR30 expressed on the mouse blastocysts, and their locations were mostly consistent with the binding sites of estrogen on the blastocyst cells. Furthermore, both estrogen and GPR30-selective agonist could induce the rapid increase of Cai2+ of blastocyst cells, while GPR30-selective antagonist could specifically block the fast effect of estrogen. Moreover, the pretreatment of G15 on blastocysts lead to a lower implantation rate, compared with that of control. Thus, it can be inferred that GPR30 can mediate the fast effect of estrogen on blastocysts and play important role in embryo implantation.