Gap junctions are important molecular supports of ependymal cell functions, and gap junction alterations have been linked to astrocyte dysfunction induced by NMO-IgG.12 To test if gap junctions are also affected by NMO-IgG in cultured ependymal cells, we analysed the effects of several NMO-IgG on the expression of Connexin 43 (Cx43), the main gap junction of ependymal cells, on primary cultures after 24 hours treatment.34 In NT cultures, Cx43 was expressed as agglomerates at the lateral membrane (Fig. 2A). Here, GJA1 is linked to neuromyelitis optica.