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Does Gabapentin Affect Neural Tube Development? Experimental Study Using an Early Stage Chick Embryo Model.

Ahmet Cetinkal1, Asli Cakir

  • 1Istanbul Medipol University, Faculty of Medicine, Department of Neurosurgery, Istanbul, Turkey.

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Summary

Gabapentin (GBP) use in early pregnancy may cause neural tube defects in developing embryos. This study found that all tested doses of GBP led to midline closure defects in chick embryos, suggesting a potential risk.

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Area of Science:

  • Developmental Biology
  • Teratology
  • Pharmacology

Background:

  • Gabapentin (GBP) is a medication with various clinical uses.
  • Its safety during early pregnancy, particularly concerning embryonic development, requires thorough investigation.
  • The early stage chick embryo (ESCE) model offers a valuable system for studying neurulation.

Purpose of the Study:

  • To evaluate the potential teratogenic effects of Gabapentin (GBP) on neural tube development.
  • To investigate the impact of different GBP doses on embryonic development in an early stage chick embryo (ESCE) model.
  • To assess the risk of GBP exposure during the critical period of first-trimester embryonic development.

Main Methods:

  • Fertile chick eggs (n=100) were divided into four groups: control, subtherapeutic, therapeutic, and supratherapeutic doses of GBP.
  • Gabapentin was administered via subblastoderm injection after 30 hours of incubation (Hamburger and Hamilton stage 9).
  • Embryos were incubated for 72 hours and subsequently examined macroscopically and histopathologically using hematoxylin eosin staining.

Main Results:

  • A significant increase in neural tube defects was observed in all GBP-treated groups compared to the control group (p<0.001).
  • The incidence of neural tube defects was 4.34% (control), 59.09% (subtherapeutic), 65.21% (therapeutic), and 81.81% (supratherapeutic).
  • All tested doses of Gabapentin were associated with midline closure defects in the ESCE model.

Conclusions:

  • Gabapentin (GBP) exposure, at all tested doses, is linked to midline closure defects in early stage chick embryos (ESCEs).
  • This study provides the first evidence of GBP-induced neural tube defects using an ESCE model.
  • Further research with larger sample sizes is warranted to elucidate the mechanisms of embryonic damage and assess effects at lower doses.