ketamine exposure during embryogenesis inhibits cellular proliferation in rat fetal cortical neurogenic regions background developmental neurotoxicity of ketamine an nmethyldaspartate receptor antagonist must be considered due to its widespread uses for sedationanalgesiaanesthesia in pediatric and obstetric settings dosedependent effects of ketamine on cellular proliferation in the neurogenic regions of rat fetal cortex ventricular zone vz and subventricular zone svz were investigated in this in vivo studymethods timedpregnant spraguedawley rats at embryonic day 17 e17 were given with different doses of ketamine intraperitoneally 0 1 2 10 20 40 and 100 mgkg proliferating cells in the rat fetal brains were labeled by injecting 100 mgkg of 5bromo2deoxyuridine brdu intraperitoneally brdulabeled cells were detected by immunostaining methods the numbers of brdupositive cells in vz and svz of rat fetal cortex were employed to quantify proliferation in the developing rat cortexresults ketamine dosedependently reduced the number of brdupositive cells in vz p 0001 and svz p 0001 of the rat fetal cortex svz showed greater susceptibility to ketamineinduced reduction of proliferation in rat fetal cortex occurring even at clinically relevant doses 2 mgkgconclusion these data suggest that exposure to ketamine during embryogenesis can dosedependently inhibit the cellular proliferation in neurogenic regions of the rat fetal cortex