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Updated: Aug 9, 2026

Neural Tube Closure in Mouse Whole Embryo Culture
07:37

Neural Tube Closure in Mouse Whole Embryo Culture

Published on: October 21, 2011

What are the molecular mechanisms of neural tube defects?

J Corcoran1

  • 1Developmental Biology Research Centre, Randall Institute, London, United Kingdom. udli155@kcl.ac.uk

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|March 21, 1998
PubMed

Insights

Inositol effectively treats folate-resistant neural tube defects (NTDs) in mouse models. This treatment may work by increasing retinoic acid receptor beta, correcting cell proliferation issues.

Area of Science:

  • Developmental biology
  • Genetics
  • Biochemistry

Background:

  • Neural tube defects (NTDs) are common congenital malformations.
  • Folic acid prevents most NTDs, but folate-resistant cases lack effective treatments.
  • The curly tail mutant mouse serves as a model for folate-resistant NTDs.

Purpose of the Study:

  • To investigate the efficacy of inositol as a treatment for folate-resistant NTDs.
  • To explore the molecular mechanisms underlying inositol's therapeutic effect.

Main Methods:

  • Administration of inositol to curly tail mutant mice.
  • Analysis of molecular pathways, including retinoic acid receptor beta expression.

Main Results:

  • Inositol administration cured neural tube defects in the curly tail mutant mouse model.
  • The proposed mechanism involves up-regulation of retinoic acid receptor beta in the hindgut endoderm.
  • This up-regulation is thought to correct a cellular proliferation defect.

Conclusions:

  • Inositol shows promise as a treatment for folate-resistant NTDs.
  • The retinoic acid pathway may be a key target for treating these resistant malformations.
  • Further research is needed to confirm these findings and explore alternative explanations.

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