Effects of folic acid and homocysteine on spinal cord morphology of the chicken embryo.

Maternal ingestion of folic acid (FA) reduces neural tube defects, which are associated with high homocysteine levels. Present study evaluated the effects of FA and homocysteine on cell proliferation and cell adhesion, as well as on apoptosis, throughout the development of the spinal cord and mesenchyme of chicken embryos. Normal closure of the neural tube and a regular distribution of the mesenchymal cells were observed in control and FA-treated embryos. All homocysteine-treated embryos and also 6 of 10 embryos treated with FA+homocysteine showed failure of closure of the neural tube. Homocysteine decreased the thickness of the mantle and marginal layers of the spinal cord, and FA did not prevent this effect. FA treatment reversed the decrease of proliferating cells in the spinal cord induced by homocysteine. FA-treated embryos showed the highest numerical density of apoptotic cells. Homocysteine treatment reduced NCAM expression in both spinal cord and mesenchymal tissue, and FA prevents this effect. These results are important because they demonstrate in situ that the imbalance between FA and homocysteine levels can lead to disruptions in spinal cord development, changing proliferation, apoptosis, and cell adhesion and consequently changing the arrangement of the spinal cord layers.