An Electrophysiological Model of Spinal Transmission Deficits in Mouse Experimental Autoimmune Encephalomyelitis

Chronic relapsing/remitting experimental autoimmune enceph-alomyelitis (EAE) can be induced in 8-week-old female SJL/ J(H-2) mice via inoculation with the p139–151 peptide of myelin proteolipid protein (PLP), Mycobacterium tuberculosis (MT), complete Freund’s adjuvant (CFA), and Bordatella pertussis. EAE is a relevant preclinical model of MS that incorporates several aspects of the clinical disease. Chief among these are the inflammatory mediated neurological deficits. While the im-pact of localized spinal cord demyelination on neurotransmis-sion has been modeled successfully, relatively little work has been done with spinal cord from animals with EAE. The goal of this study was to assess the utility of a grease-gap tissue bath methodology in the detection of transmission deficits in EAE spinal cord tissue. Spinal cords removed from EAE mice a