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Experimental autoimmune encephalomyelitis (EAE) induced by ventricular injection of antimyelin oligodendrocyte antibodies in DA rats showed severe clinical signs 4 to 5 days after injection. Immunocytochemically, connexin 43 (Cx43) expression increased in the choroid plexus and in the subventricular and subgranular zones of the hippocampus during the development of acute EAE, and decreased after the beginning of the remission phase of the disease. Quantitative computing analysis showed a significantly increased Cx43 expression in the choroid plexus at the peak of the disease. Plaque-pattern expression of the Cx43 in the choroid plexus (CP) of acute EAE correlated with the increased docking and coupling of the Cx43 hemichannels revealed by atomic force microscopy (AFM). The inner diameter of the gap junction (GJ) channels decreased in the CP of acute EAE, measured by AFM. Cell structure conformational changes showed influences the channels' flexibility in acute EAE.

Clinical signs appearance and significant increases of ICAM-1 and MMP-2 expressions with the clusters of VCAM-1(+) immunoreactivity in the choroids plexus epithelium to transferred anti-myelin oligodendroglial antibodies into the third brain ventricle, indicate important role of choroids plexus in the induction of acute experimental autoimmune encephalomyelitis (EAE). Magnetic brain stimulation with AKMA micro-magnet flux density of 60 miliTesla, 5 mm in diameter, implanted upon the pineal gland (PG), immediately after antibody injection, significantly decreases the expression of MMP-2 and ICAM-1 in the choroids plexus of the rat brain and abruptly suppresses the induction of acute EAE.