Developmental changes in diffusion anisotropy coincide with immature oligodendrocyte progression and maturation of compound action potential

Alexander Drobyshevsky, Sheng Kwei Song, Georgi Gamkrelidze, Alice M. Wyrwicz, Matthew Derrick, Fan Meng, Limin Li, Xinhai Ji, Barbara Trommer, Douglas J. Beardsley, Ning Ling Luo, Stephen Back, Sidhartha Tan

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Disruption of oligodendrocyte lineage progression is implicated in the white-matter injury that occurs in cerebral palsy. We have previously published a model in rabbits consistent with cerebral palsy. Little is known of normal white-matter development in perinatal rabbits. Using a multidimensional approach, we defined the relationship of oligodendrocyte lineage progression and functional maturation of axons to structural development of selected cerebral white-matter tracts as determined by diffusion tensor imaging (DTI). Immunohistochemical studies showed that late oligodendrocyte progenitors appear at gestational age 22 [embryonic day 22 (E22)], whereas immature oligodendrocytes appear at E25, and both increase rapidly with time (∼13 cells/mm2/d) until the onset of myelination. Myelination began at postnatal day 5 (P5) (E36) in the internal capsule (IC) and at P11 in the medial corpus callosum (CC), as determined by localization of sodium channels and myelin basic protein. DTI of the CC and IC showed that fractional anisotropy (FA) increased rapidly between E25 and P1 (E32) (∼11% per day) and plateaued (

Original languageEnglish (US)
Pages (from-to)5988-5997
Number of pages10
JournalJournal of Neuroscience
Issue number25
Publication statusPublished - Jul 22 2005



  • Brain development
  • Compound action potential
  • Conduction velocity
  • Diffusion tensor imaging
  • Oligodendrocyte
  • Sodium channel

ASJC Scopus subject areas

  • Neuroscience(all)

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