Forskolin- and cholera toxin-activated adenylate cyclase activity increases between the morula and blastocyst stages of mouse preimplantation development, as assessed by the ability of these agents to increase embryonic cAMP levels. Development of activatable adenylate cyclase requires transcription but is independent of the fifth nuclear replication, cell division, and compaction. Early cavitating embryos treated with cholera toxin and forskolin or with N6-monobutyryl-cAMP display an increase in the rate of fluid accumulation in comparison with untreated controls. The stimulatory effect is specific for cAMP, since neither the inactive cAMP analogue N6-monobutyryl-2'-deoxy-cAMP nor N2-monobutyryl-cGMP stimulates the rate of fluid accumulation. These results constitute the first report of a possible physiological function for cAMP in preimplantation development, namely, in blastocoel formation.
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