Ikeda K, Shirai S, Majima A, Hirabayashi Y, Yamada K
Department of Ophthalmology, Nagoya City University Medical School, Japan.
Jpn J Ophthalmol. 1995;39(1):20-9.
Histological and histochemical studies were carried out in Jcl:ICR mice to determine the changes in microscopic structures and glycosaminoglycan molecular species in the tissues involved in normal or faulty closure of the embryonic fissure. The purpose of this study was to elucidate the mechanism underlying the faulty closure of the embryonic fissure and to identify the key substances involved in normal and faulty closure. To obtain mice with an appropriate faulty closure of the embryonic fissure, ochratoxin A was employed as a teratogenic agent. Serial sections from tissues undergoing normal and faulty closure of the embryonic fissure were cut at a right angle to the fissure. As the staining procedures, a hematoxylin-eosin procedure and a sensitized high iron diamine method were used. A chemical modification (nitrous acid treatment) or an enzyme digestion procedure (chondroitinase ABC digestion procedure) was employed in combination with the sensitized high iron diamine method to identify the glycosaminoglycan molecular species in the tissues. The results obtained in the present study have substantiated the histophysiological importance of glycosaminoglycan molecular species during the course of histogenesis in the normal and the faulty closure of the embryonic fissure of developing murine eyes.
