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Alan C Rupp, Samer Hattar; Genetic dissection of retinal circuits underlying the pupillary light reflex. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1230.
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The pupillary light reflex (PLR) is crucial for proper visual function by regulating the amount of light entering the eye. The PLR begins with light detection in the retina; however, the retinal circuitry underlying this reflex is poorly understood. We therefore sought to identify the cell types and circuits within the retina that mediate the PLR.
To investigate the cells and retinal circuits underlying the PLR, we used a genetic silencing approach to remove the function of specific cell types within the retina. We evaluated the dark-adapted PLR in each of these mutant mouse lines in response to broad-spectrum white light similar to that in the environment.
Contrary to predictions from previous work, mutant mice lacking rod function displayed a substantial reduction in PLR sensitivity, lacking pupil constriction until the light intensity reached photopic levels. In contrast, cone mutant mice displayed no observable defects in PLR sensitivity or kinetics. Additionally, we have found that mice containing rods as the only photoreceptors have a normal PLR at all light intensities, including photopic. However, animals with cones as the only photoreceptors have only a brief, transient PLR and only at the brightest light intensities. Lastly, though the PLR requires rods, we found that the PLR persists in animals lacking the primary and secondary rod circuits.
We have uncovered a primary involvement of rods in driving the PLR across a wide range of light intensities. In addition, we have uncovered evidence of a novel rod pathway in the retina for the PLR that is distinct from the conventional rod circuits.
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