Off-like Responses to the Blue-light in rd1/ChR2 Mouse Retina

Off-like Responses to the Blue-light in rd1/ChR2 Mouse Retina
Issue Date
International Meeting on Substrate-Integrated Microelectrode Arrays
, 95-97
Optogenetics, a technique to utilize a variety of microbial opsin genes to control cellular behaviors with light, has been shown as a potential means to restore light-sensing functions in the retina of animal model of retinitis pigmentosa. One of the strategies for optogenetic vision restoration was to express channelrhodopsin (ChR2) genes to retina ganglion cells which are the only gateway for visual data transmission from retina to brain. Previous study reported that ganglion cells expressing ChR2 by Thy-1 promoter were depolarized by blue light, regardless of whether they were ON or OFF ganglion cells. In this study, however, we report that a few OFF-like ganglion cells were observed in the rd1/ChR2 mouse retina, showing decreased firing rates with blue light illumination. ChR2-eYFP was widely expressed in the rd1/ChR2 retina and the layer of outer nuclear was absent. Many ganglion cells showed increased firing rates with blue light illumination, a typical ON-like response by the direct ChR2-induced depolarization. However, a few ganglion cells with OFF-like responses were also observed with a decreased firing rate when blue light was illuminated onto the retina. The same retina sample did not respond to yellow light, indicating that OFF responses of ganglion cell was not photoreceptor-mediated but optogenetically-mediated. Treatment of GABA antagonist, picrotoxin can enhance response of ganglion cells to the optogenetic stimulation. We speculate that this OFF response may be resulted by a pathway involving amacrine cells which may suppress the ganglion cells activity by an inhibitory neurotransmitter, GABA. This speculation warrants a further study to confirm the mechanism of OFF response in rd1/ChR2 retina.
Appears in Collections:
KIST Publication > Conference Paper
Files in This Item:
There are no files associated with this item.
RIS (EndNote)
XLS (Excel)


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.