Axonal transport rate decreased at the onset of optic neuritis in EAE mice.

摘要: Optic neuritis is frequently the first symptom of multiple sclerosis (MS), an inflammatory demyelinating neurodegenerative disease. Impaired axonal transport has been considered as early event diseases. However, few studies have assessed integrity in MS or its animal models. We hypothesize that impairment occurs at onset optic experimental autoimmune encephalomyelitis (EAE) mice. In this study, we employed manganese-enhanced MRI (MEMRI) to assess nerves EAE mice neuritis. Axonal was (a) nerve Mn(2+) accumulation rate (in % signal change/h) by measuring increased total enhancement, and (b) mm/h) change length enhanced Mn(2+). Compared sham-treated healthy mice, significantly decreased 19% 38% for with moderate severe neuritis, respectively. The 43% 65% degree deficit correlated extent impaired visual function diminished microtubule-associated tubulins, well severity inflammation, demyelination, injury