Abstract
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 language | English |
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Pages (from-to) | 313-320 |
Number of pages | 8 |
Journal | Journal of Anatomy |
Volume | 186 |
Issue number | 2 |
Publication status | Published - Apr 1995 |
Keywords
- Animals
- Axons
- Disease Models, Animal
- Ethanol
- Fetal Alcohol Spectrum Disorders
- Mice
- Mice, Inbred C57BL
- Mice, Inbred CBA
- Microscopy, Electron
- Myelin Sheath
- Optic Nerve