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Function: require_once
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Function: _error_handler
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Filename: models/Detail_model.php
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Function: insertAPISummary
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File: /var/www/html/application/controllers/Detail.php
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Ectopic induction of optogenetic actuators, such as channelrhodopsin, is a promising approach to restoring vision in the degenerating retina. However, the cell type-specific response of ectopic photoreception has not been well understood. There are limits to obtaining efficient gene expression in a specifically targeted cell population by a transgenic approach. In the present study, we established a murine model with high efficiency of gene induction to retinal ganglion cells (RGCs) and amacrine cells using an improved tetracycline transactivator-operator bipartite system (KENGE-tet system). To investigate the cell type-specific visual restorative effect, we expressed the channelrhodopsin gene into RGCs and amacrine cells using the KENGE-tet system. As a result, enhancement in the visual restorative effect was observed to RGCs and starburst amacrine cells. In conclusion, a photoresponse from amacrine cells may enhance the maintained response of RGCs and further increase or improve the visual restorative effect.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10265492 | PMC |
http://dx.doi.org/10.1016/j.omtm.2023.05.011 | DOI Listing |
Function (Oxf)
December 2024
Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Korea.
During retinal visual processing, rod bipolar cells (RBC) transfer scotopic signals from rods to AII amacrine cells as second-order neurons. Elucidation of the RBC's excitation/inhibition is essential for understanding the visual signal transmission. Excitation mechanisms via mGluR6 and voltage-gated Ca2+ channels in the RBCs and GABAergic inhibitory synaptic inputs have been studied in previous studies.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2024
Committee on Computational Neuroscience, Department of Organismal Biology and Anatomy, University of Chicago, Chicago, IL 60637.
Everything that the brain sees must first be encoded by the retina, which maintains a reliable representation of the visual world in many different, complex natural scenes while also adapting to stimulus changes. This study quantifies whether and how the brain selectively encodes stimulus features about scene identity in complex naturalistic environments. While a wealth of previous work has dug into the static and dynamic features of the population code in retinal ganglion cells (RGCs), less is known about how populations form both flexible and reliable encoding in natural moving scenes.
View Article and Find Full Text PDFFront Neurosci
November 2024
Department of Ophthalmology, USC Roski Eye Institute, University of Southern California, Los Angeles, CA, United States.
Introduction: Considering the significant role played by both intrinsic and extrinsic electric fields in the growth and maturation of the central nervous system, the impact of short exposure to external electric fields on the development and differentiation of retinal organoids was investigated.
Methods: Retinal organoids derived from human embryonic stem cells were used at day 80, a key stage in their differentiation. A single 60-minute exposure to a biphasic electrical field was administered to assess its influence on retinal cell populations and maturation markers.
Through decades of research, we have gained a comprehensive understanding of the protein complexes underlying function and regulation of chemical synapses in the nervous system. Despite the identification of key molecules such as ZO-1 or CaMKII, we currently lack a similar level of insight into the electrical synapse proteome. With the advancement of BioID as a tool for proteomics, it has become possible to identify complex interactomes of a given protein of interest by combining enzymatic biotinylation with subsequent streptavidin affinity capture.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2024
Department of Neuroscience, Yale University, New Haven, CT 06511.
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