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| http://dx.doi.org/10.1523/JNEUROSCI.1399-07.2007 | DOI Listing |
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Optomotor responses are a popular way to assess sub-cortical visual responses in mice. We studied photoreceptor inputs into optomotor circuits using genetically-modified mice lacking the exocytotic calcium sensors synaptotagmin 1 (Syt1) and 7 (Syt7) in rods or cones. We also tested mice that in which cone transducin, GNAT2, had been eliminated.
View Article and Find Full Text PDFSynchronized Photoactivation of T4K Rhodopsin Causes a Chromophore-Dependent Retinal Degeneration That Is Moderated by Interaction with Phototransduction Cascade Components.
J Neurosci
September 2024
Department of Ophthalmology & Visual Sciences, University of British Columbia, Vancouver, British Columbia V5Z 3N9, Canada
Multiple mutations in the gene cause sector retinitis pigmentosa in humans and a corresponding light-exacerbated retinal degeneration (RD) in animal models. Previously we have shown that T4K rhodopsin requires photoactivation to exert its toxic effect. Here we further investigated the mechanisms involved in rod cell death caused by T4K rhodopsin in mixed male and female In this model, RD was prevented by rearing animals in constant darkness but surprisingly also in constant light.
View Article and Find Full Text PDFDark continuous noise from mutant G90D-rhodopsin predominantly underlies congenital stationary night blindness.
Proc Natl Acad Sci U S A
May 2024
Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Congenital stationary night blindness (CSNB) is an inherited retinal disease that causes a profound loss of rod sensitivity without severe retinal degeneration. One well-studied rhodopsin point mutant, G90D-Rho, is thought to cause CSNB because of its constitutive activity in darkness causing rod desensitization. However, the nature of this constitutive activity and its precise molecular source have not been resolved for almost 30 y.
View Article and Find Full Text PDFGenetic manipulation of rod-cone differences in mouse retina.
PLoS One
May 2024
Department of Ophthalmology and Stein Eye Institute, David Geffen School of Medicine, University of California, Los Angeles, California, United States of America.
Though rod and cone photoreceptors use similar phototransduction mechanisms, previous model calculations have indicated that the most important differences in their light responses are likely to be differences in amplification of the G-protein cascade, different decay rates of phosphodiesterase (PDE) and pigment phosphorylation, and different rates of turnover of cGMP in darkness. To test this hypothesis, we constructed TrUx;GapOx rods by crossing mice with decreased transduction gain from decreased transducin expression, with mice displaying an increased rate of PDE decay from increased expression of GTPase-activating proteins (GAPs). These two manipulations brought the sensitivity of TrUx;GapOx rods to within a factor of 2 of WT cone sensitivity, after correcting for outer-segment dimensions.
View Article and Find Full Text PDFLight-dependent regulation of neurotransmitter release from rod photoreceptor ribbon synapses involves an interplay of Complexin 4 and Transducin with the SNARE complex.
Front Mol Neurosci
February 2024
Animal Physiology/Neurobiology, Department of Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Article Synopsis
- Adaptation of photoreceptor sensitivity to light is crucial for vision, yet the mechanisms behind synaptic adaptation are not well understood.
- Complexin 4 plays a key role in regulating neurotransmitter release in rod photoreceptors by limiting synaptic vesicle release in response to light, enhancing light signaling at the synapse.
- A study revealed that Complexin 4 interacts with Transducin and the SNARE complex, suggesting a presynaptic mechanism that helps photoreceptors adjust to varying light conditions.
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