We showed previously that mice deficient in astrocyte gap junctions Cx43 and Cx30 exhibit white matter vacuolation and hypomyelination. In this study we tested the hypothesis that loss of astrocytic gap junction proteins leads to exacerbation of the primary demyelinating diseases, using experimental autoimmune encephalomyelitis (EAE) as a model system. To test for this, Cx43 floxed mice were crossed with GFAP:Cre, Cx30 null mice to generate mice lacking astrocytic expression of both Cx43 and Cx30 (dKO). EAE was induced using myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide, and mice were monitored for acute expression of disease. No statistically significant difference in clinical or pathological expression of EAE was observed. Lesion load and susceptibility of different areas of the CNS to inflammation were similar in all genotypes. Moreover, no differences were noted in blood-brain barrier (BBB) permeability, tissue wet weight, axonal pathology, gliosis or demyelination during acute disease. These data show that loss of the astrocytic connexins, Cx43 and Cx30, and the white matter pathology observed in these mice does not statistically affect clinical or pathological expression of EAE and show that astrocyte gap junctions do not regulate autoimmune inflammation and associated BBB disruption in acute EAE.
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