Multiple sclerosis (MS) is a chronic autoimmune disease whose symptoms are caused by an inflammatory invasion of the central nervous system (CNS). The molecular pathogenesis of MS includes an increased permeability of the blood brain barrier (BBB) along with an inability of the BBB to fulfill its normal function of protecting the CNS. The cerebellar BBB seems to be especially vulnerable, as the development of experimental autoimmune encephalomyelitis (EAE) as an animal model of MS often takes its beginning in the cerebellum. Inflammatory lesion development seems to correlate with increased permeability of the local BBB. Responsible for the BBB are cerebral and cerebellar capillary endothelial cells. We therefore generated an in vitro model of the cerebellar BBB (cerebEND) and compared its response to inflammatory stimuli (TNFalpha administration) with a cerebral BBB in vitro model (cEND) characterised previously [Förster, C., Silwedel, C., Golenhofen, N., Burek, M., Kietz, S., Mankertz, J., Drenckhahn, D., 2005. Occludin as direct target for glucocorticoid-induced improvement of blood brain-barrier properties in a murine in vitro system. J. Physiol. 565(Pt 2), 475-486]. We could demonstrate a faster and more pronounced increase in permeability in the cerebellar BBB manifested by reduced transendothelial electrical resistance and reduced tight junction protein expression. This cell line cerebEND could thus be valuable to identify genes differently expressed within the BBB in the future and therefore be helpful in finding new ways of treatment of MS.