Background: Neural tube defects are congenital malformations of the central nervous system. Genetic predisposition and some environmental factors play an important role in the development of neural tube defects. This study aimed to investigate the effects of diclofenac sodium on the neural tube development in a chick embryo model that corresponds to the first month of vertebral development in mammals. Materials and methods: Seventy-five fertile, specific pathogen-free eggs were incubated for 28 h and were divided into five groups of 15 eggs each. Diclofenac sodium was administered via the sub-blastodermic route at this stage. Incubation was continued till the end of the 48th h. All eggs were then opened and embryos were dissected from embryonic membranes and evaluated morphologically and histopathologically. Results: It was determined that the use of increasing doses of diclofenac sodium led to defects of midline closure in early chicken embryos. There were statistically significant differences in neural tube positions (open or close) among the groups. In addition; crown–rump length, somite number were significantly decreased in high dose experimental groups compared with control group. Conclusions: This study showed that development of neurons is affected in chicken embryos after administration of diclofenac sodium. The exact teratogenic mechanism of diclofenac sodium is not clear; therefore it should be investigated. (Folia Morphol 2019; 78, 2: 307–313)
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