Abstract
The death of photoreceptor cells is induced by continuous light exposure. However, it is unclear whether light damage was induced in retinal ganglion cells with photosensitivity by transduction of optogenetic genes. In this study, we evaluated the phototoxicities of continuous light exposure on retinal ganglion cells after transduction of the optogenetic gene mVChR1 using an adeno-associated virus vector. Rats were exposed to continuous light for a week, and visually evoked potentials (VEPs) were recorded. The intensities of continuous light (500, 1000, 3000, and 5000 lx) increased substantially after VEP recordings. After the final recording of VEPs, retinal ganglion cells (RGCs) were retrogradely labeled with a fluorescein tracer, FluoroGold, and the number of retinal ganglion cells was counted under a fluorescent microscope. There was no significant reduction in the amplitudes of VEPs and the number of RGCs after exposure to any light intensity. These results indicated that RGCs were photosensitive after the transduction of optogenetic genes and did not induce any phototoxicity by continuous light exposure.
Highlights
Photoreceptor degeneration is induced by exposure to continuous light or UV radiation
Evoked potentials (VEPs) were clearly recorded in the Royal College of Surgeons (RCS) rats injected with the adeno-associated virus vector (AAV)-modified volvox-derived channelrhodopsin-1 (mVChR1) after mVChR1 gene transduction (Figure 2), the Visually evoked potentials (VEPs) were not recordable in the only Venus-transduced retina
Optogenetic-mediated gene therapy for restoring vision is expected to be a treatment for patients with retinitis pigmentosa
Summary
Photoreceptor degeneration is induced by exposure to continuous light or UV radiation It is well known as light damage, and its mechanisms have been well investigated in rodents. The effectiveness and safety of optogenetic gene therapy for RP have been investigated in behavioral studies [10,11] and immunological responses [12]. Other types of channelrhodopsins, such as modified volvox-derived channelrhodopsin-1 (mVChR1) with a broad spectrum [13,14] and ChrimsonR with a redshifted spectrum [15], have been developed, and the method of optogenetic gene therapy is becoming a promising treatment for restoring vision in blind patients [16]. The present study was designed to investigate whether photosensitive RGCs were damaged by intense light exposure
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