EPENDYMAL DENUDATION, AQUEDUCTAL OBLITERATION AND HYDROCEPHALUS AFTERA SINGLE INJECTION OF NEURAMINIDASE INTO THE LATERAL VENTRICLE OF ADULT-RATS

Citation
Jm. Grondona et al., EPENDYMAL DENUDATION, AQUEDUCTAL OBLITERATION AND HYDROCEPHALUS AFTERA SINGLE INJECTION OF NEURAMINIDASE INTO THE LATERAL VENTRICLE OF ADULT-RATS, Journal of neuropathology and experimental neurology, 55(9), 1996, pp. 999-1008
Citations number
53
Categorie Soggetti
Pathology,Neurosciences,"Clinical Neurology
ISSN journal
00223069
Volume
55
Issue
9
Year of publication
1996
Pages
999 - 1008
Database
ISI
SICI code
0022-3069(1996)55:9<999:EDAOAH>2.0.ZU;2-T
Abstract
To investigate the role of sialic acid in the ependyma of the rat brai n, we injected neuraminidase from Clostridium perfingens into the late ral ventricle of 86 adult rats that were sacrificed at various time in tervals. After administration of 10 mu g neuraminidase, ciliated cuboi dal ependymal cells of the lateral ventricles, third ventricle, cerebr al aqueduct, and the rostral half of the fourth ventricle died and det ached. The ependymal regions sealed by tight juntions such as the chor oid plexus and the subcommissural organ were not affected. Debris was removed by infiltrating neutrophils and macrophagic cells. At the same time, after ependymal disappearance, the aqueduct was obliterated. In this region, mitoses were evident and cystic ependymal cells were fre quent. Hydrocephalus of the lateral and third ventricles was evident 4 days after neuraminidase injection. Gliosis was restricted to the dor sal telencephalic wall of the injected lateral ventricle. It is though t that cleavage of sialic acid from ependymal surface glycoproteins or glycolipids, likely involved in cell adhesion, led to the detaching a nd death of the ependymal cells. Thereafter, ependymal loss, together with edema, led to fusion of the lateral walls of the cerebral aqueduc t and this in turn provoked hydrocephalus of the third and lateral ven tricles. This model of experimental hydrocephalus is compared with oth er models, in particular those of hydrocephalus after viral invasion o f the cerebral ventricles.