| Background:Multiple sclerosis (MS) is an inflammatory disease of CNS characterized by focal areas of demyelination in CNS, also is a myelin antigen-specific T-cell-mediated autoimmune disease. Worldwide, approximately 1,100,000 individuals are afflicted with MS. Women with the disease outnumber men two to one. The etiology is unknown. Genetic factors may are important in the development of MS. Genome-wide studies have revealed that susceptibility to MS is linked to genes in the major histocompati bility complex (MHC) on chromosome 6. Alleles for certain class II genes, HLA-DR and HLA-DQ, confer the strongest risk of contracting MS. Both cell-mediated and humorally mediated immune mechanisms contribute to pathological injury. The pathogenesis of MS is thought to involve a T-cell-mediated autoimmune process.The munber of the glial cells constitute 90 % of the total cells in CNS, their volume constitutes nearly half of CNS. There is an increasingly important role of glial cell revealed in recent years. They can play active roles in physiological and pathological condition such as responding to stimulation, integrating afferent information, and adjusting the function of synapse conduction and modulating activation of neurons, ect. Therefore, it is of important clinical significance to investigate the relations between the glias and the mechanism of MS injury. Objectives:The aim of the present study is to investigate the response of AS, microglias and neurons in the Guinea pig model with EAE, and the changes of Cx43 and Cx32 expression in the reactived AS and neurons respectively, and the relationship between them. We will further investigate the relationship between the reactived glias and injury of EAE.Methods:1. By using immunohistochemical single or double staining method, we investigated the response of AS, GFAP as a marker, and microglia, OX42 as a marker, and the expression of Cx43 andCx32, the protein family form GJ, in the brain of guinea pig model with EAE. 2. With imrnuno-electron-microscopic staining, we investigated the ultrastructural characters of GJ between the neurons and AS, and the ultrastructural alteration of the glias and neurons in brain of guinea pig model with EAE. 3. Pre-injecting carbenoxolone (CBX), a gap junction blocker, into the lateral ventricle, we further observed the changes of OX42 and GFAP expression. Results:In guinea pig model with EAE, we obsearved that: 1. The microglias were activated in the white matter of brain with EAE. The microglial cells appeared the ramified and rod figuration in the early stages of EAE. They became amoeboid and round cells in the later stage of EAE. 2. The GFAP-Li AS proliferated, the cell bodies hypertrophied and processes thickened, these processes formed a network between each other. 3 .The Cx43-Li cells increased and manifested spot and fibre. The Cx32-Li cells also increased in the white matter of brain with EAE. 4. Immune electron microscope staining found GJ between AS. The number of the Cx43-Li of GJ was significantly increased, compared with that of the control group.5. By using pre-injecting CBX into the lateral ventricle, we observed that the GFAP expression was 504 ±55. 88 in the guinea pig group treated by CBX, while in control guinea pig group treated by physiological saline was 497 + 49. 69. The difference of GFAP-Li expression between two groups was not found (P >0.05). In guinea pig treated by CBX, the expression of OX42 was 120 ± 10.64, and in control guinea pig treated by saline was 242 + 35.35. The expression of OX42 in the...
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