Cranial effects of retinoic acid in the loop-tail ( Lp) mutant mouse.
The effects of retinoic acid (RA) on the manifestation and nature of neural tube defects (NTD) in heterozygous embryos of mutant mice carrying the gene loop-tail ( Lp) and in normal (+/+) littermates and embryos from normal homozygous matings were compared with NTD that occur in untreated abnormal homozygous ( Lp/ Lp) embryos. A single intraperitoneal dose (5 mg/kg) of RA administered at 9 AM or 3 PM on day 8 of gestation induced NTD in +/+ as well as Lp/+ embryos removed on day 12 of gestation. All of the NTD were confined to the brain and consisted of exencephaly involving the diencephalon, mesencephalon, and metencephalon. In neither phenotype ( Lp/+; +/+) was the massive exencephaly and myeloschisis characteristic of untreated Lp/ Lp embryos produced; thus, it is possible that the teratogenic mechanisms of RA-induced defects and of Lp-induced defects may differ.[1]References
- Cranial effects of retinoic acid in the loop-tail (Lp) mutant mouse. Wilson, D.B., Wyatt, D.P., Gookin, J.L. J. Craniofac. Genet. Dev. Biol. (1990) [Pubmed]
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