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

Tsen Hsuan Lin, Joong Hee Kim, Carlos Perez-Torres, Chia Wen Chiang, Kathryn Trinkaus, Anne H. Cross, Sheng Kwei Song

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Optic neuritis is frequently the first symptom of multiple sclerosis (MS), an inflammatory demyelinating neurodegenerative disease. Impaired axonal transport has been considered as an early event of neurodegenerative diseases. However, few studies have assessed the integrity of axonal transport in MS or its animal models. We hypothesize that axonal transport impairment occurs at the onset of optic neuritis in experimental autoimmune encephalomyelitis (EAE) mice. In this study, we employed manganese-enhanced MRI (MEMRI) to assess axonal transport in optic nerves in EAE mice at the onset of optic neuritis. Axonal transport was assessed as (a) optic nerve Mn2+ accumulation rate (in % signal change/h) by measuring the rate of increased total optic nerve signal enhancement, and (b) Mn2+ transport rate (in mm/h) by measuring the rate of change in optic nerve length enhanced by Mn2+. Compared to sham-treated healthy mice, Mn2+ accumulation rate was significantly decreased by 19% and 38% for EAE mice with moderate and severe optic neuritis, respectively. The axonal transport rate of Mn2+ was significantly decreased by 43% and 65% for EAE mice with moderate and severe optic neuritis, respectively. The degree of axonal transport deficit correlated with the extent of impaired visual function and diminished microtubule-associated tubulins, as well as the severity of inflammation, demyelination, and axonal injury at the onset of optic neuritis.

Original languageEnglish
Pages (from-to)244-253
Number of pages10
JournalNeuroImage
Volume100
DOIs
StatePublished - Oct 15 2014

Keywords

  • Axonal transport
  • Manganese-enhanced MRI
  • Optic neuritis

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