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Development of rod function in term born and former preterm subjects
Anne B Fulton1, Ronald M Hansen, Anne Moskowitz
1Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. anne.fulton@childrens.harvard.edu
Insights
Normal rod function development, assessed by electroretinography (ERG) and psychophysics, reveals immature central retinal function in infants. This research provides a foundation for understanding retinopathy of prematurity (ROP).
Area of Science:
- Ophthalmology
- Developmental Biology
- Neuroscience
Background:
- Rod photoreceptor function is crucial for vision, particularly in low light conditions.
- Understanding the normal developmental trajectory of rod function is essential for identifying visual impairments.
- Retinopathy of prematurity (ROP) is a significant cause of visual impairment in premature infants.
Purpose of the Study:
- To investigate the normal development of rod function using electroretinography (ERG) and psychophysical methods.
- To apply these findings to understand visual development in infants with retinopathy of prematurity (ROP).
Main Methods:
- Electroretinography (ERG) recorded rod photoreceptor sensitivity (SROD) from dark-adapted subjects.
- Biochemical modeling of phototransduction activation was used to calculate SROD from ERG a-waves.
- Psychophysical thresholds for detecting stimuli in parafoveal and peripheral retina were measured to assess rod-mediated function.
Main Results:
- In term-born infants, SROD development correlates with rhodopsin levels, and central retinal rod function matures later than peripheral function.
- In preterm infants, SROD deficits persist post-ROP resolution.
- Mild ROP prolongs the maturation of central rod-mediated visual thresholds.
Conclusions:
- Characterizing normal rod and rod-mediated visual function development provides a baseline for ROP studies.
- Deviations from normal development in ROP patients highlight specific functional deficits.
- This foundational understanding aids in diagnosing and managing visual impairments associated with ROP.
Purpose:
To provide an overview of some of our electroretinographic (ERG) and psychophysical studies of normal development of rod function and their application to retinopathy of prematurity (ROP).
Methods:
ERG responses to full-field stimuli were recorded from dark adapted subjects. Rod photoreceptor sensitivity (SROD) was calculated by fit of a biochemical model of the activation of phototransduction to the ERG a-wave. Dark adapted psychophysical thresholds for detecting 2 degrees spots in parafoveal (10 degrees eccentric) and peripheral (30 degrees eccentric) retina were measured and the difference between the thresholds, Delta10-30, was examined as a function of age. SROD and Delta10-30 in term born and former preterm subjects were compared.
Results:
In term born infants, (1) the normal developmental increase in SROD changes proportionately with the amount of rod visual pigment, rhodopsin, and (2) rod-mediated function in central retina is immature compared with that in peripheral retina. In subjects born prematurely, deficits in SROD persist long after active ROP has resolved. Maturation of rod-mediated thresholds in the central retina is prolonged by mild ROP.
Conclusions:
Characterization of the development of normal rod and rod-mediated function provides a foundation for understanding ROP.
