With regard to neurological disorders, mice lacking H3R (H3R−/−) develop more severe experimental allergic encephalomyelitis (EAE) with a marked increase of blood brain barrier permeability and an increased expression of macrophage-inflammatory protein (MIP)-2 and interferon-inducible protein-10 (IP-10/CXCL10) on peripheral T cells. This evidence concerns the gene CXCL10 and nervous system disorder.