Andrew W. Mellon Foundation Fellow in the Reproductive Sciences on leave from the Department of Anatomy, Semmelweis Medical School, Budapest, Hungary.
Ultrastructural analysis of malformations of the embryonic neural axis induced by in vitro hyperglycemic conditions
Article first published online: 26 MAY 2005
Copyright © 1985 Wiley-Liss, Inc., A Wiley Company
Volume 32, Issue 3, pages 363–373, December 1985
How to Cite
Reece, E. A., Pinter, E., Leranth, C. Z., Garcia-Segura, M., Sanyal, M. K., Hobbins, J. C., Mahoney, M. J. and Naftolin, F. (1985), Ultrastructural analysis of malformations of the embryonic neural axis induced by in vitro hyperglycemic conditions. Teratology, 32: 363–373. doi: 10.1002/tera.1420320306
- Issue published online: 26 MAY 2005
- Article first published online: 26 MAY 2005
- Manuscript Accepted: 5 JUN 1985
- Manuscript Received: 10 APR 1985
Neural tube defects are the most common malformations associated with diabetic pregnancies. Although the teratogenic effects of excess glucose have been investigated in in vivo and in vitro studies, a cellular basis for neural tube defects has not been elucidated. We used rat embryo culture to study the organogenesis period of development, with excess d-glucose added to the serum medium to induce neural tube anomalies. Light and electron microscopic examination of control 12-day-old embryos grown 48 hours in culture revealed blastlike cells with few organelles or cellular processes. Twelve-day-old embryos cultured in excess d-glucose had advanced cellular maturation with differentiation, including the presence of free polysomes and copious cell processes, regardless of whether they had an open neural tube. Cytoarchitectural changes such as decreased numbers of mitotic figures with mitotic cells in the mantle layer were focally distributed throughout the neural epithelium but with predominance at the site of failed closure. In vivo studies failed to demonstrate neural processes in day 12 normal embryos. Fourteen-day-old embryos grown in utero also had foci of cell processes in the neural tube but to a much lesser degree than that observed in the in vitro day 12 glucose-exposed embryos. The cellular aberrations in the excess d-glucose-treated embryos are characteristic of a premature maturational change. Since they are present in excess d-glucose-exposed embryos with or without failure of neural tube closure, these maturational and cytoarchitectural changes may contribute to the cellular basis for neural tube defects.