Embryonic development neural tube defects

The correct level of the active metabolites of vitamin A which control the nuclear receptor signalling pathway is required for appropriate embryonic development. Too much or too little of the receptor ligands is equally harmful for the embryo. It has been well documented that when there is an excess of vitamin A or its metabolites during embryonic development, defects occur in the CNS. An excess of RA causes specific defects of the anterior hindbrain whereby anterior rhombomeres can be lost or respecified to more posterior areas or it can cause poste-riorization of the whole CNS, whereby forebrain structures are lost [36, 50, 86-88]. More recently, Maden et al. describe defects that arise in the central nervous system of quail embryos when they develop in the absence of vitamin A [50]. There are three defects in these embryos (1) the posterior hindbrain is completely missing (2) the neural tube fails to extend neurites out into the periphery (3) the neural crest cells die. 

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