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Optic nerve hypoplasia in the fetal alcohol syndrome: a mouse model
S H Parson1, B Dhillon, G S Findlater
1Department of Anatomy, University of Edinburgh, UK.
Insights
Fetal alcohol syndrome can cause optic nerve hypoplasia. This study used a mouse model to show that alcohol exposure during pregnancy leads to a significant loss of myelinated axons in offspring optic nerves by 15 weeks.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Optic nerve hypoplasia is a common feature of fetal alcohol syndrome (FAS).
- This condition is linked to impaired vision in affected children.
- Animal models are crucial for understanding FAS-related developmental abnormalities.
Purpose of the Study:
- To investigate the effects of prenatal alcohol exposure on optic nerve development in a mouse model.
- To determine if a binge alcohol exposure model can replicate optic nerve hypoplasia observed in FAS.
- To quantify changes in optic nerve structure and myelinated axon numbers following gestational alcohol exposure.
Main Methods:
- Pregnant mice (C57BL/6 x CBA)F1 were administered a single dose of ethanol (25%) on gestational days 11 or 12.
- Offspring optic nerves were analyzed using transmission electron microscopy at 3, 6, 9, and 15 weeks of age.
- Systematic random sampling quantified optic nerve cross-sectional area and myelinated axon counts.
Main Results:
- No significant differences in optic nerve cross-sectional area or axon number were observed between control and alcohol-exposed groups from 3 to 9 weeks.
- Between 9 and 15 weeks, alcohol-exposed groups showed a ~25% loss of myelinated axons.
- A trend towards a smaller optic nerve cross-sectional area was noted in the alcohol-exposed group by 15 weeks.
Conclusions:
- Prenatal binge alcohol exposure in mice results in a progressive loss of myelinated axons in the optic nerve.
- This mouse model demonstrates a potential mechanism for optic nerve hypoplasia associated with fetal alcohol syndrome.
- The findings highlight the long-term neurotoxic effects of gestational alcohol exposure on visual pathway development.
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)