Optic nerve hypoplasia in the fetal alcohol syndrome: a mouse model

S H Parson, Baljean Dhillon, G S Findlater, M H Kaufman

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Optic nerve hypoplasia is commonly observed in children affected by the fetal alcohol syndrome, and is believed to contribute to their poor visual acuity. We have used a 'binge' model of alcohol abuse in an attempt to recreate this hypoplasia in a mouse model. Pregnant female (C57BL/6 x CBA)F1 mice were injected intraperitoneally with a single dose of a 25% solution of ethanol (v:w), either on d 11 or d 12 of gestation. Optic nerves were prepared for transmission electron microscopy from offspring at 3, 6, 9 and 15 wk of age (n = 64). A systematic random sampling technique was used to analyse both the cross-sectional areas of the optic nerves from semithin sections, and the numbers and cross-sectional areas of myelinated axons from thin sections. We found no significant differences either in the cross-sectional area or in the number of axons in the optic nerves between 3 and 9 wk from control and alcohol-treated groups. From 9 to 15 wk, alcohol-treated groups showed a loss of approximately 25% of myelinated axons (65,931 +/- 2806-49,186 +/- 3194: mean number of axons +/- S.E.M., respectively). Over the same period the number of axons in control groups was relatively stable (62,087 +/- 2043-64,703 +/- 3607). This resulted in an optic nerve with statistically significantly fewer myelinated axons at 15 wk in the alcohol-treated group, and was reflected in a trend towards a smaller cross-sectional area of the optic nerve in alcohol-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Original languageEnglish
Pages (from-to)313-20
Number of pages8
JournalJournal of Anatomy
Volume186 ( Pt 2)
Publication statusPublished - Apr 1995


  • Animals
  • Axons
  • Disease Models, Animal
  • Ethanol
  • Fetal Alcohol Spectrum Disorders
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Microscopy, Electron
  • Myelin Sheath
  • Optic Nerve

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