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Updated: May 12, 2026
A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
Prenatal hypoxia is associated with long-term retinal dysfunction in rats
Stephane L Bourque1, Sharee Kuny, Laura M Reyes
1Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Alberta, Canada.
Insights
Intra-uterine growth restriction (IUGR) in rats leads to early cone and later rod retinal dysfunction, impacting vision from young to old age. These findings highlight the long-term effects of fetal programming on retinal health.
Area of Science:
- Ophthalmology
- Developmental Biology
- Neuroscience
Background:
- Intra-uterine growth restriction (IUGR) is linked to increased susceptibility to age-related health issues.
- This study investigates if IUGR in rat models exacerbates age-related retinal dysfunction.
Purpose of the Study:
- To determine the long-term effects of IUGR on retinal function and anatomy in aging rats.
- To investigate the differential impact of IUGR on cone- and rod-driven retinal pathways.
Main Methods:
- IUGR was induced in Sprague-Dawley rats via gestational hypoxia (11.5% O2).
- Retinal function was assessed using electroretinogram (ERG) recordings at 2 and 14 months of age.
- Retinal anatomy was evaluated using immunofluorescence.
Main Results:
- Aged IUGR offspring showed significant deficits in rod-driven retinal function (a-wave, b-wave, oscillatory potentials).
- Young IUGR offspring exhibited cone-specific dysfunction (b-wave, oscillatory potentials, photopic flicker), which persisted into old age.
- Functional deficits occurred without corresponding anatomical retinal losses.
Conclusions:
- The developing retina is sensitive to prenatal stressors like hypoxia.
- Cone- and rod-driven retinal pathways have different susceptibilities to IUGR-induced dysfunction.
- Prenatal programming significantly impacts age-related retinal dystrophies, influencing diagnostic and therapeutic strategies.
Background:
Intra-uterine growth restriction (IUGR) has been associated with increased predisposition to age-related complications. We tested the hypothesis that rat offspring models of IUGR would exhibit exacerbated, age-related retinal dysfunction.
Methods:
Female Sprague-Dawley rats (maintained at 11.5% O2 from gestational day 15 to 21 to induce IUGR) and control offspring (maintained at 21% O2 throughout pregnancy) had retinal function assessed at 2 months (young) and 14 months of age (aged) with electroretinogram (ERG) recordings. Retinal anatomy was assessed by immunofluorescence.
Results:
Deficits in rod-driven retina function were observed in aged IUGR offspring, as evidenced by reduced amplitudes of dark-adapted mixed a-wave V(max) (by 49.3%, P < 0.01), b-wave V(max) (by 42.1%, P < 0.001) and dark-adapted peak oscillatory potentials (by 42.3%, P < 0.01). In contrast to the rod-driven defects specific to aged IUGR offspring, light adapted ERG recordings revealed cone defects in young animals, that were stationary until old age. At 2 months, IUGR offspring had amplitude reductions for both b-wave (V(max) by 46%, P < 0.01) and peak oscillatory potential (V(max) by 38%, P < 0.05). Finally, defects in cone-driven responses were further confirmed by reduced maximal photopic flicker amplitudes at 2 (by 42%, P < 0.001) and 14 months (by 34%, P = 0.06) and critical flicker fusion frequencies at 14 months (
Control:
42 ± 1 Hz, IUGR: 35 ± 2 Hz, P < 0.05). These functional changes were not paralleled by anatomical losses in IUGR offspring retinas.
Conclusions:
These data support that the developing retina is sensitive to stressors, and that pathways governing cone- and rod-driven function differ in their susceptibilities. In the case of prenatal hypoxia, cone- and rod-driven dysfunction manifest at young and old ages, respectively. We must, therefore, take into account the specific impact that fetal programming might exert on age-related retinal dystrophies when considering related diagnoses and therapeutic applications.
