Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina

Abstract Targeting the photosensitive ion channel channelrhodopsin‐2 (ChR2) to the retinal circuitry downstream of photoreceptors holds promise in treating vision loss caused by retinal degeneration. However, the high intensity of blue light necessary to activate channelrhodopsin‐2 exceeds the safet...

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Main Authors: Abhishek Sengupta, Antoine Chaffiol, Emilie Macé, Romain Caplette, Mélissa Desrosiers, Maruša Lampič, Valérie Forster, Olivier Marre, John Y Lin, José‐Alain Sahel, Serge Picaud, Deniz Dalkara, Jens Duebel
Format: Article
Language:English
Published: Springer Nature 2016-09-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201505699
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author Abhishek Sengupta
Antoine Chaffiol
Emilie Macé
Romain Caplette
Mélissa Desrosiers
Maruša Lampič
Valérie Forster
Olivier Marre
John Y Lin
José‐Alain Sahel
Serge Picaud
Deniz Dalkara
Jens Duebel
author_facet Abhishek Sengupta
Antoine Chaffiol
Emilie Macé
Romain Caplette
Mélissa Desrosiers
Maruša Lampič
Valérie Forster
Olivier Marre
John Y Lin
José‐Alain Sahel
Serge Picaud
Deniz Dalkara
Jens Duebel
author_sort Abhishek Sengupta
collection DOAJ
description Abstract Targeting the photosensitive ion channel channelrhodopsin‐2 (ChR2) to the retinal circuitry downstream of photoreceptors holds promise in treating vision loss caused by retinal degeneration. However, the high intensity of blue light necessary to activate channelrhodopsin‐2 exceeds the safety threshold of retinal illumination because of its strong potential to induce photochemical damage. In contrast, the damage potential of red‐shifted light is vastly lower than that of blue light. Here, we show that a red‐shifted channelrhodopsin (ReaChR), delivered by AAV injections in blind rd1 mice, enables restoration of light responses at the retinal, cortical, and behavioral levels, using orange light at intensities below the safety threshold for the human retina. We further show that postmortem macaque retinae infected with AAV‐ReaChR can respond with spike trains to orange light at safe intensities. Finally, to directly address the question of translatability to human subjects, we demonstrate for the first time, AAV‐ and lentivirus‐mediated optogenetic spike responses in ganglion cells of the postmortem human retina.
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institution Kabale University
issn 1757-4676
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language English
publishDate 2016-09-01
publisher Springer Nature
record_format Article
series EMBO Molecular Medicine
spelling doaj-art-754898926dc74e3a8b3a6c9af06db69b2025-08-20T03:43:30ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-09-018111248126410.15252/emmm.201505699Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retinaAbhishek Sengupta0Antoine Chaffiol1Emilie Macé2Romain Caplette3Mélissa Desrosiers4Maruša Lampič5Valérie Forster6Olivier Marre7John Y Lin8José‐Alain Sahel9Serge Picaud10Deniz Dalkara11Jens Duebel12INSERM, U968INSERM, U968INSERM, U968INSERM, U968INSERM, U968INSERM, U968INSERM, U968INSERM, U968School of Medicine, University of TasmaniaINSERM, U968INSERM, U968INSERM, U968INSERM, U968Abstract Targeting the photosensitive ion channel channelrhodopsin‐2 (ChR2) to the retinal circuitry downstream of photoreceptors holds promise in treating vision loss caused by retinal degeneration. However, the high intensity of blue light necessary to activate channelrhodopsin‐2 exceeds the safety threshold of retinal illumination because of its strong potential to induce photochemical damage. In contrast, the damage potential of red‐shifted light is vastly lower than that of blue light. Here, we show that a red‐shifted channelrhodopsin (ReaChR), delivered by AAV injections in blind rd1 mice, enables restoration of light responses at the retinal, cortical, and behavioral levels, using orange light at intensities below the safety threshold for the human retina. We further show that postmortem macaque retinae infected with AAV‐ReaChR can respond with spike trains to orange light at safe intensities. Finally, to directly address the question of translatability to human subjects, we demonstrate for the first time, AAV‐ and lentivirus‐mediated optogenetic spike responses in ganglion cells of the postmortem human retina.https://doi.org/10.15252/emmm.201505699channelrhodopsinoptogeneticsprimateretinavision restoration
spellingShingle Abhishek Sengupta
Antoine Chaffiol
Emilie Macé
Romain Caplette
Mélissa Desrosiers
Maruša Lampič
Valérie Forster
Olivier Marre
John Y Lin
José‐Alain Sahel
Serge Picaud
Deniz Dalkara
Jens Duebel
Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
EMBO Molecular Medicine
channelrhodopsin
optogenetics
primate
retina
vision restoration
title Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
title_full Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
title_fullStr Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
title_full_unstemmed Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
title_short Red‐shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina
title_sort red shifted channelrhodopsin stimulation restores light responses in blind mice macaque retina and human retina
topic channelrhodopsin
optogenetics
primate
retina
vision restoration
url https://doi.org/10.15252/emmm.201505699
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