Combined Mouse Retinal Optoretinography/Electroretinography System to Study Light-Evoked Responses in Animal Models...

To study the correlation between optoretinogram (ORG) and the underlying phototransduction-initiated physiology, we irradiated mouse retinas with visible light centered at a 482-nm wavelength to induce bleach-initiated morphologic changes in the outer retinal layers, including photoreceptors and the retinal pigment epithelium (RPE).

A 482-nm light-emitting diode was used for short-pulse irradiation of the retina over a large field of view in the three groups of mice, including disease models, while acquiring optical coherence tomography (OCT) image sequences using a custom-built OCT system combined with a commercial electroretinogram (ERG) system. The visible light exposure was adjusted to vary the total light energy (number of photons) delivered to the retina, enabling observation of the bleach-level dependence of the ORG and ERG signals.

Light-driven thickness increments in the outer retinal layers, including the photoreceptors and RPE, were observed in wild-type (WT) albino and pigmented mice. However, the energy of light stimuli did not produce a response in the retina of the rd10 mouse model. The lack of a full-field ERG response in the same animals also confirmed this observation. These suggested that phototransduction in the 3-month-old rd10 mice could not be initiated.

The ORG and ERG measurements recorded under various light stimuli reveal the retina's neural function. The ORG and ERG signals from the WT albino and pigmented mice exhibited thickness increments in the ORG and an increase in amplitude of a-waves and b-waves in the ERG, which were linked to phototransduction; however, these signal trends were not observed in the rd10 mice. Therefore, the ORG/ERG system could be an attractive instrument that provides both localized structural and global functional information about the investigated retina, allowing for detailed studies of neural function suppression in animal models of retinal degeneration.