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B. Kashyap, L. C. Frederickson, D. L. Stenkamp; Ethanol Induced Microphthalmia in Zebrafish During Retinal Neurogenesis - A Search for Mechanisms. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3071.
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© ARVO (1962-2015); The Authors (2016-present)
In zebrafish, embryonic ethanol exposure results in features comparable to those seen in human fetal alcohol syndrome (FAS; Bilotta et al., 2004 Neurotoxicol Teratol. Nov-Dec;26(6):737-43). One of the common visual phenotypes in human FAS is microphthalmia. In this study we examine cellular aspects of this microphthalmic phenotype following ethanol exposure during retinal neurogenesis. We also pursue a mechanism implicated in pathogenesis of FAS, reduced retinoic acid (RA) signaling.
1) Embryos were exposed to 1.5% ethanol during a 24 hour period corresponding to retinal neurogenesis. Eye sizes were measured, and cell-specific markers were applied to retinal cryosections. 2) To reduce RA signaling, embryos were treated with an inhibitor of retinaldehyde dehydrogenase, diethylaminobenzaldehyde (DEAB) over the same time frame, and eye sizes were measured. 3) Rescue experiments were carried out with 0.3uM RA added together with 1.5% ethanol.
1) Ethanol exposure during the time of retinal neurogenesis results in subsequent and persistent microphthalmia. Our histological findings suggest that this is due to a combination of general developmental delay, increased cell death in the lens, and decreased retinal cell differentiation. 2) DEAB treatment also results in microphthalmia. 3) Preliminary findings suggest that co-treatment of embryos with RA may attenuate ethanol induced microphthalmia.
Ethanol exposure during retinal neurogenesis causes selective effects on the retina and lens, resulting in persistent microphthalmia. Ethanol induced microphthalmia may in part be mediated by inhibition of RA signaling. This study provides insight into the mechanisms underlying microphthalmia as a consequence of embryonic ethanol exposure.
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