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Endothelial NMDA Receptor Involvement in Retinal Neurovascular Damage Following Prenatal Alcohol Exposure in a Mouse
Anaïs Leroy1, Audrey Valentin1, Camille Sautreuil1
1Univ Rouen Normandie, INSERM U1245, Team Epigenetics and Pathophysiology of Neurodevelopmental Disorders, Rouen F-76000, France.
Prenatal alcohol exposure causes fetal alcohol spectrum disorders by damaging brain and eye development. This study shows that blocking NMDA receptors in endothelial cells prevents alcohol-induced retinal vascular defects and neuronal damage.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Prenatal alcohol exposure (PAE) leads to fetal alcohol spectrum disorders (FASD), causing neurodevelopmental damage.
- PAE disrupts brain and ocular development, affecting vasculature and neuronal positioning.
- NMDA receptors (NMDARs) are implicated in FASD, with altered expression and function.
Purpose of the Study:
- To investigate the role of endothelial NMDAR (eNMDAR) in retinal vascular development.
- To determine if eNMDAR mediates PAE-induced retinal neurovascular defects.
- To characterize the neurovascular phenotype in mice lacking eNMDAR under PAE conditions.
Main Methods:
- Utilized an in vivo mouse model of FASD.
- Employed transgenic mice lacking the endothelial GluN1 subunit of NMDAR (eNMDAR knockout).
- Analyzed retinal vascular plexus development and neuronal cell density and positioning.
Main Results:
- Deletion of eNMDAR mimicked PAE-induced defects in superficial vascular plexus progression.
- eNMDAR knockout prevented some PAE-induced retinal vascular impairments.
- Loss of eNMDAR increased calretinin-positive interneurons contacting vessels and protected against PAE-induced decrease.
Conclusions:
- Endothelial NMDARs are crucial for normal retinal neurovascular development.
- eNMDARs mediate, at least partially, the adverse effects of ethanol on the developing retina.
- Targeting eNMDAR may offer a strategy to mitigate PAE-induced retinal damage in FASD.
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