FLUORESCENCE LOCALIZATION OF ANTI-PREGNANT RAT-KIDNEY ANTIBODY AND LECTIN-BINDING ANALYSIS IN EXENCEPHALIC RAT EMBRYOS

Citation
M. Fujii et al., FLUORESCENCE LOCALIZATION OF ANTI-PREGNANT RAT-KIDNEY ANTIBODY AND LECTIN-BINDING ANALYSIS IN EXENCEPHALIC RAT EMBRYOS, Child's nervous system, 12(10), 1996, pp. 595-603
Citations number
24
Categorie Soggetti
Clinical Neurology",Pediatrics
Journal title
ISSN journal
02567040
Volume
12
Issue
10
Year of publication
1996
Pages
595 - 603
Database
ISI
SICI code
0256-7040(1996)12:10<595:FLOARA>2.0.ZU;2-9
Abstract
We sought to determine the distribution of anti-pregnant rat kidney se rum (ARKS) in fetuses that subsequently developed a form of neural tub e defect (NTD). We produced exencephaly in rat embryos by injecting a rabbit anti-pregnant rat kidney serum into the peritoneal cavity of pr egnant Wistar rats on day 7 of gestation; 71.1% (27/38) of the rat emb ryos developed this anomaly. Fluorescence immunohistochemical studies were performed to localize ARKS binding in the embryos. We also invest igated the binding of two lectins, concanavalin A (ConA) and wheat ger m agglutinin (WGA), to glycoconjugates on neuroepithelium during the p rocess of neurulation in rat embryos injected with normal rabbit serum (NRS) and ARKS. We found for the first time that ARKS directly affect ed the neural tube during neurulation. Intense fluorescence was observ ed on the luminal side of the neuroepithelium in the intercellular reg ion and on the basement membrane of the neural tube in embryos on day 9 of gestation (GD9). In GD21 embryos there was much more intense fluo rescence in the extracellular matrix and the ependymal lining cells of the ventricles than in controls. The binding of the two lectins on th e cell surface of the neuroepithelium during neurulation was different in rat embryos injected with ARKS than in normal embryos injected wit h NRS. These results support the idea that simple nonclosure and overg rowth constitute the mechanism of NTD. However, the lectin-binding dat a suggest that dysraphic states may be induced by cell-to-cell adhesiv e molecular failure.