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Pathogenesis of Ochratoxin A‐ and Concanavalin A‐Induced Exencephalies in Mice
Author(s) -
HAYASAKA Ikuo,
HOSHINO Kiyoshi,
KAMEYAMA Yoshiro
Publication year - 1986
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.1986.tb00654.x
Subject(s) - exencephaly , neural tube , neuroepithelial cell , neural crest , mesenchyme , neural fold , embryo , biology , pathogenesis , neurulation , anatomy , pathology , microbiology and biotechnology , neural plate , embryogenesis , medicine , teratology , immunology , neural stem cell , gastrulation , fetus , stem cell , pregnancy , genetics
Early morphogenetic changes of exencephaly induced by ochratoxin A (OA) were compared with those induced by concanavalin A (Con A) in mice in order to examine possible differences in the pathogenesis of neural tube defect. OA and Con A were administered to pregnant mice on day 7 of gestation, and the process of neural tube closure of embryos was observed at different times from 6 to 72 hours after treatment by SEM and light microscopy. In OA‐treated embryos, the cranial neural folds in the fore‐ and midbrains did not elevate and remained in the biconvex shape. The cellular changes were found in the neuroepithelium and surface ectoderm. Neural crest cells, which appeared at the lateral edges of the neural folds, were also involved in degeneration. In Con A‐treated embryos, the neural folds in the mid‐ and hindbrains elevated to assume the V shape, but remained wide open. The main cellular change was a degeneration of the primary mesenchyme underlying the neuroepithelium, resulting in a paucity of the supporting mesenchymal tissue. These findings suggest that the exencephalies produced by either OA or Con A are primarily due to non‐closure of the neural tube, but that the pathogenesis differs with each agent. Failure of neural tube closure in OA‐treated embryos appears to result from damage of the neuroepithelium and neural crest cells, whereas that in Con A‐treated embryos from damage of the primary mesenchyme.