For in vivo studies we modified an established, passive-transfer mouse model of NMO in which intracerebral administration of AQP4-IgG and human complement by stereotaxic infusion produces characteristic NMO pathology with loss of AQP4 and GFAP, complement deposition, inflammation and demyelination, but with minimal axonal damage. This evidence concerns the gene AQP4 and neuromyelitis optica.