title: Diffusion tensor imaging detected optic nerve injury correlates with decreased compound action potentials after murine retinal ischemia.
abstract: OBJECTIVE
  This study evaluated the function of mouse optic nerves after transient retinal ischemia using in vitro electrophysiologic recordings of compound action potentials (CAPs) correlated with diffusion tensor imaging (DTI) injury markers with confirmation by immunohistochemistry-determined pathology.
  
  
  METHODS
  Retinal ischemia was induced in 7- to 8-week-old female C57BL/6 mice by elevating intraocular pressure to 110 mm Hg for 60 minutes. At 3 and 7 days after retinal ischemia, optic nerves were removed for CAP measurements. The CAP amplitude was recorded using suction electrodes in isolated control and injured optic nerves followed by ex vivo DTI evaluation. After DTI, optic nerves were embedded in paraffin and cut for immunohistochemical analyses.
  
  
  RESULTS
  Consistent with previous in vivo DTI measurements, a 25% decrease in axial diffusivity with normal radial diffusivity was seen at 3 days after retinal ischemia, suggesting axonal injury without myelin damage. At 7 days, there was no additional change in axial diffusivity compared with that at 3 days, but radial diffusivity significantly increased by 50%, suggestive of significant myelin damage due to sustained axonal injury. The relative anisotropy (RA) progressively decreased after retinal ischemia when compared with that of the controls. The CAP amplitude in injured nerves also progressively decreased after retinal ischemia, which correlated with the reduced RA (r = 0.80).
  
  
  CONCLUSIONS
  This study suggests that CAP amplitude reflects both axonal and myelin integrity and RA is an optimal parameter for functional assessment compared with axial or radial diffusivity alone in murine optic nerves after retinal ischemia.
authors.affiliation: Departments of Mechanical Engineering and Materials Science, Washington University, Saint Louis, Missouri 63110, USA.
authors.forename: Qing
authors.initials: Q
authors.lastname: Wang
authors.forename: Roman
authors.initials: R
authors.lastname: Vlkolinsky
authors.forename: Mingqiang
authors.initials: M
authors.lastname: Xie
authors.forename: Andre
authors.initials: A
authors.lastname: Obenaus
authors.forename: Sheng-Kwei
authors.initials: SK
authors.lastname: Song
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001369:Axons / Q000473:pathology; D056324:Diffusion Tensor Imaging; D004195:Disease Models, Animal; D004594:Electrophysiology; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D004676:Myelin Basic Protein / Q000378:metabolism; D009186:Myelin Sheath / Q000473:pathology; D009410:Nerve Degeneration / Q000473:pathology; D009901:Optic Nerve Diseases / Q000209:etiology / Q000473:pathology*; D015427:Reperfusion Injury / Q000150:complications* / Q000503:physiopathology; D012164:Retinal Diseases / Q000150:complications* / Q000503:physiopathology; D012165:Retinal Ganglion Cells / Q000473:pathology
chemical_list: D004676:Myelin Basic Protein