Abstract
Mouse blastocysts were recovered from the uterus during experimental delay of implantation and following reactivation by estradiol and progesterone. The blastocysts were exposed to 7 different ferritin-conjugated lectins and then processed for EM. Binding of the lectins to the surface of the trophoblast was assessed by visualization of the ferritin particles using transmission electron microscopy. All lectins that have been previously shown to bind to trophoblast of predelay blastocysts also bound to blastocysts during delay and after reactivation from delay. The lectin from D. biflorus (DBA), which does not bind to predelay blastocysts, began to bind to blastocysts as early as 24 h after ovariectomy and bound consistently throughout the duration of delay (5 days). Between 18-22 h after the administration of estradiol-17.beta. and progesterone for reactivation (given on the 5th day of delay, i.e., day 10 postcoitus [p.c.]), DBA binding sites disappeared from the surface of the trophoblast as the blastocysts became adherent to the uterine epithelium. Binding of DBA to delayed blastocysts was inhibited by N-acetylgalactosamine (NAcGal) and also by treatment with N-acetylgalactosaminidase prior to exposure to the lectin. Apparently, NAcGal becomes available for DBA binding during delayed implantation and is subsequently cleaved off the glycocalyx or masked by the acquisition of other molecules that prevent binding of DBA following reactivation and during subsequent implantation of the mouse blastocysts. Since DBA binding was observed before the blastocysts became completely dormant and also after they became metabolically reactivated, DBA binding is probably not directly related to the state of implantation delay. Abolition of DBA binding occurred coincident with the blastocyst''s adherence to the uterine epithelium and may be associated with the acquisition of adhesiveness.
Keywords