Neural tissue continues its maturation at the site of neural tube closure defects: implications for prenatal intervention in human samples

Childs Nerv Syst. 2004 May;20(5):313-20. doi: 10.1007/s00381-004-0950-2. Epub 2004 Apr 7.

Abstract

Objective: Our objective was to investigate the relation between the embryological development and neural tissue maturation at the site where the neural plate failed to form a neural tube.

Material and methods: Samples from 15 aborted human fetuses with neural tube defects (NTD). All of the fetuses were between 20 and 25 gestational weeks old. Indicators of neural tissue maturation, formation of basal lamina, expression of integrins and neuron specific class III beta tubulin (tuj1) were investigated. To detect the adverse effects of the environment, if any, p53 and bcl-2 activity at both sites of the open and closed neural plate were investigated as well.

Results: No difference was found in the expression of maturation-related molecules at the site of the neural plate that remained open compared with the site where the neural tube is normally formed. While high p53 activity was noted in neural tissue at the site of the neural tube defect, no such activity was detected in the neural tissue where the neural tube is normally formed.

Conclusion: Our results suggested that maturation and differentiation of neural tissue continued regardless of the failure of neural tube closure. Therefore, the neurological deficits that are encountered in NTD patients should be related to secondary damage such as amnion fluid toxicity, uterus contractions, labor, etc. It seems valuable to save the neural plate before the negative effects of the environment renders the neural tissue functionless.

MeSH terms

  • Embryonic and Fetal Development
  • Fetus / metabolism
  • Fetus / pathology
  • Humans
  • Integrin alpha2beta1 / metabolism
  • Integrin alpha3 / metabolism
  • Integrin beta1 / metabolism
  • Nerve Tissue / embryology*
  • Nerve Tissue / pathology
  • Neural Tube Defects / embryology*
  • Neural Tube Defects / pathology
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Tissue Distribution
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Integrin alpha2beta1
  • Integrin alpha3
  • Integrin beta1
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53