MATERIAL and METHODS: Sixty fertilized eggs with an average weight of 65 ± 2 g were incubated in 60%?70% humidity at 37.2°C ± 0.1°C. After 26 hours of incubation, the control group (n=12) received 0.1 mg/kg physiologic saline (S), group 1 (n=12) received 0.1 mg/kg Dex, group 2 (n=12) received 1 mg/kg Dex, and group 3 (n=12) received 5 mg/kg Dex into each embryonic disc. The eggs were incubated until Hamburger?Hamilton stage (HH) 15, HH18, and HH20. Then, the embryos were dissected and evaluated both macroscopically and microscopically.

RESULTS: The mortality rate in the control group, group 1, and groups 2 and 3 was 27%, 48%, and 100%, respectively. The neural tube thicknesses in group 1 significantly increased in HH 15 and HH20 (p<0.05). The mitosis number in group 1 significantly decreased in each stage (p<0.05). Wnt-1 expression was significantly lower in group 1 in HH15 (p<0.05) and HH18 (p<0.05), but there was no significant difference in HH20 (p>0.05). Fibroblast growth factor (FGF) expression was significantly lower in group 1 in HH15 (p<0.05). The expression of N-cadherin was significantly higher in group 1 in HH20 (p<0.05). Fibronectin expression decreased in group 1 in HH18 (p<0.01).

CONCLUSION: Although the Dex treatment did not result in neural tube closure defect, the mortality rates and neural tube thicknesses increased, whereas mitotic activation and Wnt-1 and FGF signal pathways reduced in some stages. Keywords : Primary neurulation, Secondary neurulation, Neural crest cells, Dexamethasone, Chick embryo