Related Experiment Video
Updated: Sep 20, 2026
Dual Labeling of Neural Crest Cells and Blood Vessels Within Chicken Embryos Using ChickGFP Neural Tube Grafting and Carbocyanine Dye DiI Injection
Published on: May 28, 2015
Homocysteine interference in neurulation: a chick embryo model
L A Afman1, H J Blom, N M J Van der Put
1Department of Pediatrics, University Medical Center Nijmegen, The Netherlands. L.Afman@cukz.umcn.nl
Insights
Elevated homocysteine levels may disrupt embryonic neural tube closure. An in vitro chick embryo model showed homocysteine transiently delays neural tube closure, suggesting a role in neurulation defects.
Area of Science:
- Developmental biology
- Teratology
- Embryology
Background:
- Neural tube defects (NTDs) are reduced by folic acid.
- Elevated plasma homocysteine is linked to NTDs.
- Homocysteine may be teratogenic, interfering with neural tube closure.
Purpose of the Study:
- To establish a chick embryo model for studying homocysteine's interference with neural tube closure.
- To investigate the teratogenic potential of homocysteine on embryonic development.
Main Methods:
- Chick embryos were treated with homocysteine or saline in ovo and in vitro.
- In vitro treatment occurred during a specific somite window (4-6 somites).
- Embryos were monitored for malformations and neural tube closure.
Main Results:
- In ovo homocysteine caused malformations but not increased NTDs.
- In vitro homocysteine induced dose-dependent widening and closure delay of neural pores.
- Neural tube closure was eventually completed after 16 hours in vitro.
Conclusions:
- The in vitro chick embryo model is suitable for studying homocysteine's effects on neurulation.
- Disturbed homocysteine metabolism may interfere with normal neural tube development.
Background:
Periconceptional folic acid supplementation reduces the occurrence and recurrence risk of neural tube defects (NTD). Mothers of children with NTD have elevated plasma homocysteine levels. Administering homocysteine to chick embryos is reported to cause 27% NTD. Therefore, elevated plasma homocysteine levels per se or a disturbed homocysteine metabolism may be teratogenic to the embryo and may interfere with neural tube closure. Our aim was to obtain a chick embryo model to explore the interference of homocysteine in neural tube closure.
Methods:
Homocysteine or saline was administered to chick embryos in ovo at 3 hr, 30 hr, and 60 hr of incubation and harvested at 74 hr. Homocysteine was then applied to chick embryos in vitro at a defined time window of four to six somites and followed for 6 hr.
Results:
Homocysteine administration to chick embryos in ovo resulted in several malformations but not in an increased number of NTDs. Homocysteine administration to chick embryos in vitro resulted in a transient, dose-dependent widening of the anterior neuropore and closure delay of the rhombencephalic neuropore. After 16 hr of incubation the neural tube was closed.
Conclusions:
The in vitro chick embryo model appears a good model to explore the interference of a disturbed homocysteine metabolism in neurulation.
