抽象的

Reactive Glia and Proliferation of Ependyma in Guinea Pigs with Experimental Allergic Encephalomyelitis.

Mohamed Noorulla and GC Sensharma

Experimental allergic encephalomyelitis (EAE) is a cell mediated autoimmune disease in animals, comparable to some of the spontaneously occurring human demyelinating diseases like multiple sclerosis (MS), and disseminated perivascular encephalomyelitis, as a useful working model for investigating demyelinating processes and the associated neuropathogenesis. EAE was induced in the adult healthy guinea pigs by weekly intradermal injections of homologous whole brain and spinal cord antigen together with complete Freund’s adjuvant in the ratio of 1:1 into the foot pad of the animal. The animals after injection were observed for clinical features of the disease. The clinical severity of the animals was assessed by the standard method of Keith and McDermott (1980). EAE is characterized by inflammation and demyelination. Onset of the disease symptoms appeared between day 9 and 14 after first injection. The extent of latent period was found to be 9 to 14 days after first injection. The clinical severity of the disease progressed on the succeeding days, marked by inflammatory lesions of different severity followed by perivascular demyelination in the neuraxis. The fibres in the demyelinating lesions were demyelinated with relatively well preserved axons and adjacent neurons in the grey matter. Different grades of astrocytosis were observed around the lesion sites. The astrocytes increase in number and some of them were hypertrophied. After the myelin break down, the demyelinated zones were studded with astrocytes, probably could provide only a supportive framework to the naked axons in the absence of oligodendrocytes. The ependyma lining the central canal of a few segments of the spinal cord and lining the fourth ventricle became stratified. Reactive astrogliosis, whereby astrocytes undergo varying morphological changes, is a ubiquitous but poorly understood hallmark of all central nervous system pathologies. The possible involvement of glial proliferation and their morphological aspects is discussed.