Aim:We aimed to determine whether using gabapentin (GBP), especially in the first maternal trimester, would affect the neural tube development of embryos in an early stage chick embryo (ESCE) model.
Material and Methods:One hundred fertile specific pathogen-free (SPF) chick eggs were used to investigate neurulation; they were divided into four groups of 25 eggs (Groups A, B, C, and D including control, subtherapeutic, therapeutic, and supratherapeutic dose subjects, respectively). After 30 h of incubation, all eggs reached the ninth stage of embryonic development, as defined by Hamburger and Hamilton. GBP was administered through the subblastoderm, and the eggs were incubated for 72h. The embryos were macroscopically and histopathologically investigated with hematoxylin eosin following incubation and extraction.
Results:In the 72nd hour of the study, a total of 6 eggs showed no embryo development. In groups A, B, C, and D, 1 (4.34%), 13 (59.09%), 15 (65.21%), and 18 (81.81%) neural tube defective embryos, respectively, were detected. Statistically, the difference between the groups was significant, especially in the comparisons of all GBP groups to the control group (p˂0.001) (SPSS for Windows v 23.0). However, there was no significant difference between groups B, C, and D. Additionally, we suggest that at all doses, GBP could cause neural tube defects in the ESCE.
Conclusion:Based on these results, we concluded that GBP use at any dose led to midline closure defects in ESCEs. This is the first report in the literature on GBP using an ESCE model. However, further investigations with a larger sample size are required to assess its effect at lower doses and to determine the mechanisms of embryonic damage.
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