Larsson K S, Marsk L, Svanberg-Larsson A, Tesh J M
Biol Neonate. 1977;31(1-2):51-9. doi: 10.1159/000240943.
The maternal influence on induced cleft palate frequency, as revealed by reciprocal crosses, was investigated after treatment with triamcinolone or cortisone. Mouse blastocysts from the CBA and A/Jax strains were transferred to pseudopregnant A/Jax and CBA foster mothers and in addition CBA X A/Jax and A/Jax X CBA embryos were raised in pseudopregnant CBA foster mothers. According to the period of maximum sensitivity revealed by a time response study triamcinolone was injected as a single dose (2 mg/kg, i.m.) on day 11 at 8 a.m. when the precocious development of transferred fetuses had been taken into account. A predominant uterine factor slightly modified by the fetal genome was found. This was in contrast to the effect of the 4-day treatment with cortisone (62.5 mg/kg i.m.) where, as also previously has been shown, cytoplasmic factors in the embryos were accountable for the magnitude of the teratogenic response. An increased corticoid elimination from the resistant CBA fetuses might explain the maternal influence on triamcinolone treatment but would not be responsible for the influence on cortisone-induced cleft palate frequency.