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Optic nerve hypoplasia in fetal alcohol syndrome: an update
M D Pinazo-Duran1, J Renau-Piqueras, C Guerri
1Institute of Cytological Research and Investigation Center, University Hospital La Fe, Valencia, Spain.
Insights
Prenatal alcohol exposure can cause optic nerve hypoplasia in children. Animal studies show alcohol exposure leads to reduced optic nerve size and lasting retinal damage, highlighting alcohol
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Optic nerve hypoplasia (ONH) is observed in infants exposed to alcohol in utero.
- Alcohol is a known teratogen with potential to cause developmental abnormalities.
Purpose of the Study:
- To investigate the effects of prenatal and postnatal alcohol exposure on optic nerve development in an animal model.
- To determine if alcohol-induced optic nerve damage is permanent.
Main Methods:
- Rats were exposed to alcohol via a liquid diet during gestation and lactation.
- Optic nerve size, cellular structure, and axonal integrity were assessed at various developmental stages.
- Histological and ultrastructural analyses were performed on optic nerve and retinal tissues.
Main Results:
- Alcohol-exposed rats exhibited significantly smaller optic nerves compared to controls from gestational day 21 onwards.
- Histological examination revealed altered glial cells, degenerating axons, and atrophic myelin sheaths in alcohol-exposed optic nerves.
- Reduced ganglion cell and axonal densities, along with ultrastructural damage, persisted into adulthood, indicating long-lasting effects.
Conclusions:
- Prenatal and postnatal alcohol exposure induces significant dysmorphia and irremediable damage to the optic nerve and retina.
- Alcohol acts as a teratogenic agent, leading to developmental abnormalities such as optic nerve hypoplasia.
- The observed damage has long-lasting consequences, emphasizing the critical need to avoid alcohol consumption during pregnancy.
Abstract:
Optic nerve hypoplasia was detected in up to one half of a group of Swedish children born to alcoholic mothers. Using an experimental model of pre- and postnatal alcohol exposure in rats fed a liquid diet, reduced optic nerve size from gestational day 21 (294 +/- 26 x 10(2) microns2 vs 502 +/- 16 x 10(2) microns2; n = 6; p < or = 0.001) to later in development was observed as a result of the daily mean blood alcohol levels achieved in dams and their offspring. Altered glial cells and degenerating and atrophic optic axons, myelin sheaths and ganglion cells were frequent in the alcohol-exposed optic nerves. Smaller optic nerve (1.918 +/- 61 x 10(2) microns2 vs 2.195 +/- 40 x 10(2) microns2; n = 4; p < or = 0.001), reduced gaglion cell and axonal densities, and ultrastructural damage to the macroglial cells and myelin sheaths were also detected in the treated group. All these changes remained in the retina and optic nerve of the oldest rats, as a consequence of the long-lasting effects of prenatal alcohol exposure. In summary, alcohol as a major teratogenic agent may induce dysmorphogenesis and irremediable damage to the retina and optic nerve, which frequently manifests itself as hypoplastic optic nerve.