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. 2018 Feb 7;11:9. doi: 10.3389/fnmol.2018.00009

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Copyright © 2018 Shi, Li, Chen, Xia, Li, Zhang, Xu, Li, Zhou and Song.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Ketamine exposure results in neurocristopathies. Upon ketamine exposure from stage 7 to stage 13.5. (A) Embryos exhibit shortened axis, faded trunk pigment (red arrowhead), and deficient eyes (blue arrowhead) at tailbud stage and severity of phenotypes are in a dose-dependent manner. (B) Sections of eyes in ketamine-treated embryos revealed a more rounding shape pigment, disorganized arrangement of cells (DAPI staining), reduced expression of β-tubulin III compared with the control group. Ketamine exposure also causes embryos to develop a mega-colon like phenotype (C), and cranial cartilage atrophy (D). GCL, ganglionic cell layer; INL, inner nuclear layer; ONL, outer nuclear layer; L, lens; Mk, Meckel’s cartilage; ch, ceratohyal cartilage; bh, basihyal cartilage; ba, branchial cartilage. Numbers in (A,D) indicate ketamine exposure concentration (mM) to embryos. Scale bar: (A–C) 100 μm, (D) 1 mm.