CD-1 mouse fertility rapidly declines and is accompanied with early pregnancy loss under conventional housing conditions.

CD-1 mice are commonly employed as a research model for defining mechanisms controlling early mammalian development and for understanding environmental impacts on mammalian fertility. CD-1 female mice were kept four to eight months under conventional animal care housing, and were fed ad libitum with normal laboratory mouse chow. Female weight, mating success, oocyte morphology, blastocyst development in vivo and in vitro, and RT-qPCR analysis of trophectoderm cell markers (Cdx2, Slc2a1, and Atp1a1 transcript abundance, and CDX2 localization) were assessed and contrasted with outcomes from four-week-old control CD-1 mice. Embryo development in vivo in four to eight-month-old mice was significantly reduced compared to four-week-old controls. Oocytes and blastocysts from four to eight-month-old CD-1 mice displayed high levels of fragmentation and degradation, significantly reduced embryo cell counts, decreased Cdx2 transcript abundance, and number of CDX2 positive cells in morulae. We have discovered that female CD-1 mice housed under conventional conditions display a rapid loss of fecundity as they age over a few months. Paradoxically, embryo loss can be avoided by placing early embryos collected from four to eight-month-old mice into culture to support development to the blastocyst stage. We conclude that oocyte quality rapidly declines in CD-1 female mice housed under conventional animal care conditions. Thus, four to eight-month-old female CD-1 mice represent a very distinct research model from that of younger mice and this older research animal model may be preferred for understanding environmental and physiological influences limiting fertility in women.