Suppression of clinical weakness in experimental autoimmune encephalomyelitis associated with weight changes, and post-decapitation convulsions after intracisternal-ventricular administration of 6-hydroxydopamine

摘要: Selective depletion of central nervous system norepinephrine (NE) by the neurotoxin 6-hydroxydopamine (6-OHDA) in rats subsequently inoculated with myelin basic protein (MBP) and complete Freund's adjuvant (CFA) produced experimental autoimmune encephalomyelitis (EAE) without usual expected degree weakness. The preservation strength occurred spite continued weight loss. Post-decapitation myoclonic convulsive kick latency number, which are known to depend on spinal cord NE, agreed well weakness through clinical disease course. only difference between EAE groups was that stronger 6-OHDA pretreated animals did not have an elevated pons-medulla NE compared saline intracisternal-ventricular (i.c.v.) controls. We conclude can influence course interfering noradrenergic activity independent other features associated EAE. This effect may be exerted alteration blood-spinal barrier function and/or blood flow.