Common hierarchies of susceptibility to the induction of neural tube defects in mouse embryos by valproic acid and its 4-propyl-4-pentenoic acid metabolite

Teratology ◽  
1988 ◽  
Vol 38 (4) ◽  
pp. 313-320 ◽  
Author(s):  
Richard H. Finnell ◽  
Gregory D. Bennett ◽  
Steven B. Karras ◽  
Virginia K. Mohl
Keyword(s):  
Valproic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Acid Metabolite

Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro

2002 ◽  
Vol 16 (6) ◽  
pp. 619-621 ◽  
Author(s):  
Melanie C. Fisher ◽  
Steven H. Zeisel ◽  
Mei-Heng Mar ◽  
Thomas W. Sadler
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Choline Metabolism

RNA-Seq analysis reveals candidate genes that may explain neural tube defects in mouse embryos lacking SR-BI

Placenta ◽  
2017 ◽  
Vol 51 ◽  
pp. 118-119
Author(s):  
N. Santander ◽  
C. Lizama ◽  
A. Quiroz ◽  
A. Rigotti ◽  
D. Busso
Keyword(s):  
Candidate Genes ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Rna Seq

Neural tube development in mutant (curly tail) and normal mouse embryos: the timing of posterior neuropore closure in vivo and in vitro

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 151-167
Author(s):  
A. J. Copp ◽  
M. J. Seller ◽  
P. E. Polani
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Injection Technique ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Mechanisms Of Development ◽  
Delayed Closure

A dye-injection technique has been used to determine the developmental stage at which posterior neuropore (PNP) closure occurs in normal and mutant curly tail mouse embryos. In vivo, the majority of non-mutant embryos undergo PNP closure between 30 and 34 somites whereas approximately 50% of all mutant embryos show delayed closure, and around 20% maintain an open PNP even at advanced stages of development. A similar result has been found for embryos developing in vitro from the headfold stage. Later in development, 50–60% of mutant embryos in vivo develop tail flexion defects, and 15–20% lumbosacral myeloschisis. This supports the view that delayed PNP closure is the main developmental lesion leading to the appearance of caudal neural tube defects in curly tail mice. The neural tube is closed in the region of tail flexion defects, but it is locally overexpanded and abnormal in position. The significance of these observations is discussed in relation to possible mechanisms of development of lumbosacral and caudal neural tube defects. This paper constitutes the first demonstration of the development of a genetically induced malformation in vitro.

Sign in / Sign up

Export Citation Format

Share Document