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Updated: Jul 19, 2026
In Ovo Electroporation in Embryonic Chick Retina
Published on: February 5, 2012
The effect of in ovo ethanol exposure on retina and optic nerve in a chick embryo model system
A Cevik Tufan1, Gulcin Abban, Ilgaz Akdogan
1Department of Histology and Embryology, Pamukkale University, School of Medicine, Denizli, Turkey. actufan@pau.edu.tr
Insights
Prenatal ethanol (EtOH) exposure in chick embryos caused dose-dependent retinal degeneration and optic nerve hypoplasia. Ultrastructural analysis revealed impaired myelinization and cell death, highlighting EtOH
Area of Science:
- Developmental biology
- Neuroscience
- Toxicology
Background:
- Ocular anomalies in fetal alcohol syndrome (FAS) indicate alcohol's sensitivity during ocular development.
- Prenatal alcohol exposure is a known teratogen with significant health implications for newborns.
Purpose of the Study:
- To investigate the effects of in ovo ethanol (EtOH) exposure on retinal development and optic nerve myelination at an ultrastructural level.
- To establish a chick embryo model for studying prenatal alcohol's impact on the visual system.
Main Methods:
- Fertilized chicken eggs were injected with varying doses of EtOH (0-50%) or saline (control) into the air sac.
- Embryos were incubated, and on day 20, viability, growth, optic cups, and optic nerves were assessed.
- Specimens were processed for light and electron microscopy (EM) to analyze retinal and optic nerve structures.
Main Results:
- EtOH exposure significantly reduced embryo viability and caused dose-dependent prenatal growth retardation.
- Retinal degeneration and optic nerve hypoplasia were observed, with a dose-dependent decrease in myelinated nerve fibers.
- Ultrastructural analysis revealed thinner, disorganized myelin sheaths, vacuolar structures, and signs of cell death in the retina and optic nerve.
Conclusions:
- Prenatal EtOH exposure adversely affects retinal development, specifically pigment epithelium, inner plexiform layer, and ganglion cell layer.
- Optic nerve myelination is a critical target of prenatal alcohol exposure, with observed defects including myelin thinning and disorganization.
- The study suggests that EtOH impacts retinal melanin pigmentation and optic nerve myelination, potentially through mechanisms inducing cell death.
Abstract:
Ocular anomalies seen in children with fetal alcohol syndrome (FAS) suggest that ocular structures are sensitive to alcohol exposure during their development. This study was designed to investigate the effect of in ovo ethanol (EtOH) exposure on retinal development and myelinization of optic nerve fibers at an ultra structural level in a chick embryo model system. Prior to incubation, fertilized chicken eggs were injected once with 100 microl of either 0.9% NaCl (vehicle control), or EtOH solutions at different doses (10, 30, or 50%, v:v in 0.9% NaCl) into their air sacs and incubated at 37.5 degrees C and saturation humidity. On day 20 embryos were analyzed in terms of their viability and growth and the optic cups including the optic nerves were dissected out. Specimens were processed for electron microscopy (EM). Results showed that, EtOH significantly decreased the viability of chick embryos (P < 0.045), and caused significant prenatal growth retardation (P < 0.004) in a dose-dependant manner. Light microscopy of semi thin sections revealed that prenatal exposure to EtOH resulted in both retinal degeneration and optic nerve hypoplasia (P < 0.001) in a dose-dependant manner. EM revealed that a dose-dependant decrease in the number of myelinated nerve fibers was profound in groups exposed to EtOH (P < 0.001). Furthermore, the myelin coats observed were thinner than those seen in control embryos. In groups exposed to EtOH myelin sheets were unorganized and contained vacuolar structures in between them. The tissue in between the cells and optic nerve fibers, on the other hand, lost its intact appearance with vacuolar and vesicular structures in between them. In addition, the optic nerve fibers contained granular accumulations in EtOH exposed groups. A dose dependent degeneration was also observed in retinas of EtOH exposed groups. The effect of EtOH was profound in pigment epithelium (PE), inner plexiform layer (IPL), and ganglion cell layer (GC). Mitochondrial deficiencies, and alterations in melanin granule number and distribution dominated the defects seen in PE. On the other hand, EM findings of all the affected layers were suggestive of induced cell death in EtOH exposed groups. Thus, this study suggests retinal development with the emphasis on melanin pigmentation in PE and optic nerve myelinization as potential targets of prenatal EtOH exposure and discusses potential mechanisms of EtOH action on these tissues.
