Abstract
Objective: Neural tube defects are one of the congenital malformations of the central nervous system. Although the factors that cause the development of neural tube defects and their mechanisms of action are still not clearly explained, genetic predisposition, drug use and some environmental factors are thought to play a role. In this study, it was aimed to investigate the effects of zuclopenthixol acetate (ZA) on neural tube development in a chick embryo model.
 Methods: Fourty specific pathogen-free (SPF) eggs were used in the study. The eggs were incubated for 28 hours and divided into four groups of 10 eggs each. At the end of the 28th hours, saline was injected to the control group, while ZA was administered subblastodermically to the experimental groups in 3 different doses (0.7, 1.4, 2.1 mg/kg). At the end of the 48th hours, all the eggs were opened and the embryos were dissected from the embryonic membranes and evaluated morphologically and histopathologically.
 Results: When the study groups were evaluated according to the neural tube positions (open or closed), it was found that the neural tube patency increased depending on the ZA dose, which was statistically significant (p < 0.05). In addition, morphological developments of embryos were evaluated. Compared to the control group, a statistically significant decrease was observed in the mean somite numbers in all ZA-treated groups, while a significant decrease was found in the mean cranio-caudal length only in the high-dose group.
 Conclusion: In this study, it was observed that neural tube and morphological development were adversely affected in the groups treated with ZA in the chick embryo model. It was shown that neural tube closure defects in embryos increased in direct proportion with ZA doses. However, we believe that it will not be possible to fully adapt the results of this study, which was carried out in the chick embryo model, to humans and that more comprehensive research should be conducted.
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