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Updated: Aug 2, 2025
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Published on: July 13, 2014
In Utero Alcohol Exposure Impairs Retinal Angiogenesis and the Microvessel-Associated Positioning of Calretinin
Marion Dumanoir1, Anaïs Leroy1, Delphine Burel1,2
1Rouen Université Institut National de la Santé et de la Recherche Médicale Unité 1245, Genomic and Personalized Medicine in Cancer and Neurological Disorders, Institute for Research and Innovation in Biomedicine (IRIB), Normandie University, 76183, Rouen, France.
Insights
Prenatal alcohol exposure (PAE) disrupts fetal eye development, impairing retinal vascular growth and neurovascular interactions. Ophthalmological exams may aid early detection of alcohol-related neurodevelopmental defects.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- Prenatal alcohol exposure (PAE) causes significant brain abnormalities.
- The retina, an accessible part of the central nervous system, is also affected by PAE.
- Understanding PAE's impact on retinal development can identify early diagnostic markers for fetal alcohol spectrum disorder (FASD).
Purpose of the Study:
- To characterize morphometric and cellular changes in retinal microvasculature and neurovascular interactions in a mouse model of FASD.
- To investigate the effects of PAE on vascular plexus development, angiogenesis, and neurovascular associations in the developing retina.
Main Methods:
- Utilized a mouse model of fetal alcohol spectrum disorder (FASD).
- Performed fine morphometric and cellular analysis of retinal microvasculature.
- Examined neurovascular interactions, specifically the association between calretinin-positive interneurons and microvessels.
Main Results:
- PAE significantly impaired superficial vascular plexus development, decreasing vascular migration front progression.
- Reduced vessel density and fewer perforating vessels were observed in PAE retinas, indicating inhibited angiogenesis.
- PAE disrupted the close association between migrating calretinin-positive interneurons and retinal microvessels, altering amacrine cell projections.
Conclusions:
- PAE negatively impacts retinal microvasculature development and critical neurovascular interactions.
- Ophthalmological examination of alcohol-exposed infants may reveal neurovascular defects, aiding early FASD diagnosis.
- Further research into the neurovascular contribution to alcohol's developmental effects is warranted.
Abstract:
In addition to brain disorders, which constitute a devastating consequence of prenatal alcohol exposure (PAE), eye development is also significantly affected. Given that the retina is a readily accessible part of the central nervous system, a better understanding of the impact of ethanol on retinal development might provide ophthalmological landmarks helpful for early diagnosis of fetal alcohol syndrome. This study aimed to provide a fine morphometric and cellular characterization of the development of retinal microvasculature and neurovascular interactions in a mouse model of fetal alcohol spectrum disorder (FASD). The data revealed that PAE impaired superficial vascular plexus development. In particular, progression of the vascular migration front was significantly decreased in PAE retinas, supporting a delay in plexus progression. Moreover, a significant decrease in the vessel density and number of perforating vessels was quantified in PAE mice, supporting less angiogenesis. The present study provides also the first evidence of a close interaction between migrating calretinin-positive interneurons and perforating microvessels in the inner nuclear layer of the developing retina. This neurovascular association was significantly impaired by PAE. Moreover, projections of amacrine cells were abnormally distributed and densified in stratum S1 and S2. In humans, comparison of a five-month-old control infant with a three-month-old alcohol-exposed case revealed a similar mispositioning of calretinin-positive interneurons. This opens new research avenues regarding a neurovascular contribution in the deleterious effects of alcohol in the developing retina and support that ophthalmological examination could become a promising approach for early detection of alcohol-exposed infants presenting with neurovascular brain defects.
