Relevant bibliographies by topics / Retinal Cone Photoreceptor Cells

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Retinal Cone Photoreceptor Cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 January 2023

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Journal articles on the topic "Retinal Cone Photoreceptor Cells"

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LINBERG, KENNETH A., TSUTOMU SAKAI, GEOFFREY P. LEWIS, and STEVEN K. FISHER. "Experimental retinal detachment in the cone-dominant ground squirrel retina: Morphology and basic immunocytochemistry." Visual Neuroscience 19, no. 5 (September 2002): 603–19. http://dx.doi.org/10.1017/s095252380219506x.

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The cellular responses of the cone-dominant ground squirrel retina to retinal detachment were examined and compared to those in rod-dominant species. Retinal detachments were made in California ground squirrels. The retinas were prepared for light, electron, and confocal microscopy. Tissue sections were labeled with antibodies to cone opsins, rod opsin, glial fibrillary acidic protein (GFAP), vimentin, synaptophysin, cytochrome oxidase, and calbindin D 28K. Wax sections were probed with the MIB-1 antibody to detect proliferating cells. By 10 h postdetachment many photoreceptor cells in the ground squirrel already show structural signs of apoptosis. At 1 day many photoreceptors have collapsed inner segments (IS), yet others still have short stacks of outer segment discs. At 3 days there is a marked increase in the number of dying photoreceptors. Rod and medium-/long-wavelength opsins are redistributed in the cell membrane to their synaptic terminals. At 7 days photoreceptor cell death has slowed. Some regions of the outer nuclear layer (ONL) have few photoreceptor somata. IS remnants are rare on surviving photoreceptors. At 28 days these trends are even more dramatic. Retinal pigmented epithelium (RPE) cells do not expand into the subretinal space. The outer limiting membrane (OLM) appears flat and uninterrupted. Müller cells remain remarkably unreactive; they show essentially no proliferation, only negligible hypertrophy, and there is no increase in their expression of GFAP or vimentin. Horizontal cells show no dendritic sprouting in response to detachment. The speed and extent of photoreceptor degeneration in response to detachment is greater in ground squirrel than in cat retina—only a small number of rods and cones survive at 28 days of detachment. Moreover, the almost total lack of Müller cell and RPE reactivity in the ground squirrel retina is a significant difference from results in other species.
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Bok, Dean. "Cell biology of retinal photoreceptors and pigment epithelium." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 794–95. http://dx.doi.org/10.1017/s0424820100155943.

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Retinal photoreceptors (rods and cones) and retinal pigment epithelium (RPE) are highly-polarized cells that reside in close association within the eye. They carry out their interactions from a time early in embryologic life until the demise of the organism. RPE cells position their basal surfaces on an elaborate membrane (Bruch's membrane) which is intercalated between this epithelial monolayer and the photoreceptor blood supply. Their apical surfaces face the light-sensitive organelles (outer segments) of the photoreceptors. Interactions between photoreceptors and RPE take place at this interface.Mechanisms underlying photoreceptor phototransduction are now understood to a significant degree. When a photon is absorbed by a rod or cone photopigment, its chromophore, 11-cis retinaldehyde (11-cis retinal), isomerizes to the all trans form (t-retinol) and the protein undergoes a conformational change as well. The latter event activates a retina-specific GTPase (a G-protein called transducin) which, in turn, activates a retina-specific cGMP phosphodiesterase (cGMP-PDE). This cGMP-PDE then reduces the intracellular levels of cGMP which results in the closure of Na+/Ca++ channels in the photoreceptor outer segment plasma membrane. The cell hyperpolarizes as a result and release of neurotransmitter at the synaptic terminal is diminished.
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Ozaki, Ema, Luke Gibbons, Nuno GB Neto, Paul Kenna, Michael Carty, Marian Humphries, Pete Humphries, et al. "SARM1 deficiency promotes rod and cone photoreceptor cell survival in a model of retinal degeneration." Life Science Alliance 3, no. 5 (April 20, 2020): e201900618. http://dx.doi.org/10.26508/lsa.201900618.

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Retinal degeneration is the leading cause of incurable blindness worldwide and is characterised by progressive loss of light-sensing photoreceptors in the neural retina. SARM1 is known for its role in axonal degeneration, but a role for SARM1 in photoreceptor cell degeneration has not been reported. SARM1 is known to mediate neuronal cell degeneration through depletion of essential metabolite NAD and induction of energy crisis. Here, we demonstrate that SARM1 is expressed in photoreceptors, and using retinal tissue explant, we confirm that activation of SARM1 causes destruction of NAD pools in the photoreceptor layer. Through generation of rho−/−sarm1−/− double knockout mice, we demonstrate that genetic deletion of SARM1 promotes both rod and cone photoreceptor cell survival in the rhodopsin knockout (rho−/−) mouse model of photoreceptor degeneration. Finally, we demonstrate that SARM1 deficiency preserves cone visual function in the surviving photoreceptors when assayed by electroretinography. Overall, our data indicate that endogenous SARM1 has the capacity to consume NAD in photoreceptor cells and identifies a previously unappreciated role for SARM1-dependent cell death in photoreceptor cell degeneration.
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Baden, T., and D. Osorio. "The Retinal Basis of Vertebrate Color Vision." Annual Review of Vision Science 5, no. 1 (September 15, 2019): 177–200. http://dx.doi.org/10.1146/annurev-vision-091718-014926.

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The jawless fish that were ancestral to all living vertebrates had four spectral cone types that were probably served by chromatic-opponent retinal circuits. Subsequent evolution of photoreceptor spectral sensitivities is documented for many vertebrate lineages, giving insight into the ecological adaptation of color vision. Beyond the photoreceptors, retinal color processing is best understood in mammals, especially the blueONsystem, which opposes short- against long-wavelength receptor responses. For other vertebrates that often have three or four types of cone pigment, new findings from zebrafish are extending older work on teleost fish and reptiles to reveal rich color circuitry. Here, horizontal cells establish diverse and complex spectral responses even in photoreceptor outputs. Cone-selective connections to bipolar cells then set up color-opponent synaptic layers in the inner retina, which lead to a large variety of color-opponent channels for transmission to the brain via retinal ganglion cells.
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Larison, K. D., and R. Bremiller. "Early onset of phenotype and cell patterning in the embryonic zebrafish retina." Development 109, no. 3 (July 1, 1990): 567–76. http://dx.doi.org/10.1242/dev.109.3.567.

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The regular arrangement of retinal cone cells in a mosaic pattern is a common feature of teleosts. In the zebrafish, Brachydanio rerio, the retinal cone mosaic comprises parallel rows consisting of a repeating motif of four cone types. In order to elucidate the temporal and spatial aspects of the genesis of the cone mosaic in the developing retina, we generated a monoclonal antibody that specifically binds to the double cone photoreceptor of the adult. We first saw staining in the developing retina with this antibody, FRet 43, at 48 hours postfertilization, the time at which the first photoreceptor cells undergo their final mitotic division. We then injected embryonic fish with the thymidine analog, 5-bromo-2′-deoxyuridine (BrdU), confirming with a double-labeling experiment that the onset of FRet 43 antigenicity occurs within three hours of the cellular division that generates the double cone photoreceptors. Then we stained tangential sections of the 54-hour embryonic retina with FRet 43, further showing that cells devoid of staining alternate with stained pairs of cells in a pattern that is consistent with the arrangement of photoreceptors in the adult cone mosaic. These results indicate that a marker of the double cone phenotype is expressed at approximately the same time as cellular birthday and that the mosaic patterning is present within 6 hours of this expression.
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BARNARD, ALUN R., JOANNE M. APPLEFORD, SUMATHI SEKARAN, KRISHNA CHINTHAPALLI, AARON JENKINS, MATHEAS SEELIGER, MARTIN BIEL, et al. "Residual photosensitivity in mice lacking both rod opsin and cone photoreceptor cyclic nucleotide gated channel 3 α subunit." Visual Neuroscience 21, no. 5 (September 2004): 675–83. http://dx.doi.org/10.1017/s0952523804215024.

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The mammalian retina contains three classes of photoreceptor. In addition to the rods and cones, a subset of retinal ganglion cells that express the putative sensory photopigment melanopsin are intrinsically photosensitive. Functional and anatomical studies suggest that these inner retinal photoreceptors provide light information for a number of non-image-forming light responses including photoentrainment of the circadian clock and the pupil light reflex. Here, we employ a newly developed mouse model bearing lesions of both rod and cone phototransduction cascades (Rho−/−Cnga3−/−) to further examine the function of these non-rod non-cone photoreceptors. Calcium imaging confirms the presence of inner retinal photoreceptors inRho−/−Cnga3−/−mice. Moreover, these animals retain a pupil light reflex, photoentrainment, and light induction of the immediate early genec-fosin the suprachiasmatic nuclei, consistent with previous findings that pupillary and circadian responses can employ inner retinal photoreceptors.Rho−/−Cnga3−/−mice also show a light-dependent increase in the number of FOS-positive cells in both the ganglion cell and (particularly) inner nuclear layers of the retina. The average number of cells affected is several times greater than the number of melanopsin-positive cells in the mouse retina, suggesting functional intercellular connections from these inner retinal photoreceptors within the retina. Finally, however, while we show that wild types exhibit an increase in heart rate upon light exposure, this response is absent inRho−/−Cnga3−/−mice. Thus, it seems that non-rod non-cone photoreceptors can drive many, but not all, non-image-forming light responses.
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Jaroszynska, Natalia, Philippa Harding, and Mariya Moosajee. "Metabolism in the Zebrafish Retina." Journal of Developmental Biology 9, no. 1 (March 15, 2021): 10. http://dx.doi.org/10.3390/jdb9010010.

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Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches.
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Irie, Shoichi, Rikako Sanuki, Yuki Muranishi, Kimiko Kato, Taro Chaya, and Takahisa Furukawa. "Rax Homeoprotein Regulates Photoreceptor Cell Maturation and Survival in Association with Crx in the Postnatal Mouse Retina." Molecular and Cellular Biology 35, no. 15 (May 18, 2015): 2583–96. http://dx.doi.org/10.1128/mcb.00048-15.

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TheRaxhomeobox gene plays essential roles in multiple processes of vertebrate retina development. Many vertebrate species possessRaxandRax2genes, and different functions have been suggested. In contrast, mice contain a singleRaxgene, and its functional roles in late retinal development are still unclear. To clarify mouse Rax function in postnatal photoreceptor development and maintenance, we generated conditional knockout mice in whichRaxin maturing or mature photoreceptor cells was inactivated by tamoxifen treatment (RaxiCKO mice). WhenRaxwas inactivated in postnatalRaxiCKO mice, developing photoreceptor cells showed a significant decrease in the level of the expression of rod and cone photoreceptor genes and mature adult photoreceptors exhibited a specific decrease in cone cell numbers. In luciferase assays, we found that Rax and Crx cooperatively transactivateRhodopsinandcone opsinpromoters and that an optimum Rax expression level to transactivate photoreceptor gene expression exists. Furthermore, Rax and Crx colocalized in maturing photoreceptor cells, and their coimmunoprecipitation was observed in cultured cells. Taken together, these results suggest that Rax plays essential roles in the maturation of both cones and rods and in the survival of cones by regulating photoreceptor gene expression with Crx in the postnatal mouse retina.
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HANZLICEK, BRETT W., NEAL S. PEACHEY, CHRISTIAN GRIMM, STEPHANIE A. HAGSTROM, and SHERRY L. BALL. "Probing inner retinal circuits in the rod pathway: A comparison of c-fos activation in mutant mice." Visual Neuroscience 21, no. 6 (November 2004): 873–81. http://dx.doi.org/10.1017/s0952523804216078.

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We have used wild-type mice and mice possessing defects in specific retinal circuits in order to more clearly define functional circuits of the inner retina. The retina of the nob mouse lacks communication between photoreceptors and depolarizing bipolar cells (DBCs). Thus, all light driven activity in the nob mouse is mediated via remaining hyperpolarizing bipolar cell (HBC) circuits. Transducin null (Trα−/−) mice lack rod photoreceptor activity and thus remaining retinal circuits are solely generated via cone photoreceptor activity. Activation in inner retinal circuits in each of these mice was identified by monitoring light-induced expression of an immediate early gene, c-fos. The number of cells expressing c-fos in the inner retina was dependent upon stimulus intensity and was altered in a systematic fashion in mice with known retinal mutations. To determine whether c-fos is activated via circuits other than photoreceptors in the outer retina, we examined c-fos expression in tulp1−/− mice that lack photoreceptors in the outer retina; these mice showed virtually no c-fos activity following light exposure. Double-labeling immunohistochemical studies were carried out to more clearly define the population of c-fos expressing amacrine cells. Our results indicate that c-fos may be used to map functional circuits in the retina.
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Simões, Bruno F., Filipa L. Sampaio, Ellis R. Loew, Kate L. Sanders, Robert N. Fisher, Nathan S. Hart, David M. Hunt, Julian C. Partridge, and David J. Gower. "Multiple rod–cone and cone–rod photoreceptor transmutations in snakes: evidence from visual opsin gene expression." Proceedings of the Royal Society B: Biological Sciences 283, no. 1823 (January 27, 2016): 20152624. http://dx.doi.org/10.1098/rspb.2015.2624.

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In 1934, Gordon Walls forwarded his radical theory of retinal photoreceptor ‘transmutation’. This proposed that rods and cones used for scotopic and photopic vision, respectively, were not fixed but could evolve into each other via a series of morphologically distinguishable intermediates. Walls' prime evidence came from series of diurnal and nocturnal geckos and snakes that appeared to have pure-cone or pure-rod retinas (in forms that Walls believed evolved from ancestors with the reverse complement) or which possessed intermediate photoreceptor cells. Walls was limited in testing his theory because the precise identity of visual pigments present in photoreceptors was then unknown. Subsequent molecular research has hitherto neglected this topic but presents new opportunities. We identify three visual opsin genes, rh1 , sws1 and lws , in retinal mRNA of an ecologically and taxonomically diverse sample of snakes central to Walls' theory. We conclude that photoreceptors with superficially rod- or cone-like morphology are not limited to containing scotopic or photopic opsins, respectively. Walls' theory is essentially correct, and more research is needed to identify the patterns, processes and functional implications of transmutation. Future research will help to clarify the fundamental properties and physiology of photoreceptors adapted to function in different light levels.
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Dissertations / Theses on the topic "Retinal Cone Photoreceptor Cells"

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Bumsted, Keely Maureen. "The role of opsin expression in the development of photoreceptor topography and synapses in the fetal primate retina /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/5679.

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Dunn, Felice Audris. "Gain control of rod and cone vision in the mammalian retina /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10642.

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Kennedy, Matthew James. "Turning off the light response in rod and cone photoreceptors /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9217.

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Rubin, Glen R. "Comparisons between behavioral and electrophysiological measures of visual function in rodent models of retinal degeneration." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/rubin.pdf.

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McDougal, David H. "The role of melanopsin containing retinal ganglion cells in the pupillary responses of human and non-human primates." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/mcdougal.pdf.

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Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.
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Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.
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Huang, Daming. "Molecular determinants of cGMP-binding to chicken cone photoreceptor phosphodiesterase /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5095.

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Mencl, Stine [Verfasser], and Eberhart [Akademischer Betreuer] Zrenner. "Mechanisms of cone photoreceptor cell death in models for inherited retinal degeneration / Stine Mencl ; Betreuer: Eberhart Zrenner." Tübingen : Universitätsbibliothek Tübingen, 2013. http://d-nb.info/1162843748/34.

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Aslam, Sher A. "Investigating treatment options for battlefield retinal laser injury." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:0f3677ac-90d2-4e38-86cd-9d514d3d9755.

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Battlefield retinal laser injury is an infrequent but potentially devastating cause of irreversible blindness. Resultant laser-induced photoreceptor death may occur by necrosis or apoptosis, the latter which is a form of programmed cell death that may be physiological or pathological. Though necrosis cannot be prevented, apoptosis may be inhibited under certain conditions. Therefore, following retinal laser injury, specific treatment aims to target apoptotic photoreceptors and may take the form of neuroprotection or cell replacement. The primary aim of this thesis was to construct an in vivo model in which to observe the effects of retinal laser exposure on cone photoreceptor apoptosis. Current methodology to determine the effects involves histological techniques and is therefore limited to being cross-sectional. An in vivo model would permit longitudinal study to observe the cone response to injury using clinically relevant applications, including fundus autofluorescence imaging. Such a construct would enable more sensitive evaluation of new therapies which would be of direct translational relevance. The secondary aim was to investigate potential therapeutic options for retinal laser injury by pharmacological means in the form of CNTF or cell transplantation. To identify the possible molecular signals involved in neurotrophic factor-induced photoreceptor cell survival, apoptotic gene expression was investigated focusing on those genes modulated by the CNTF pathway.
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Books on the topic "Retinal Cone Photoreceptor Cells"

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International, Symposium on Retinal Degenerations (10th 2002 Bürgenstock Switzerland). Retinal degenerations: Mechanisms and experimental therapy. New York: Kluwer Academic/Plenum Publishers, 2003.

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M, LaVail Matthew, Hollyfield Joe G, and Anderson Robert E, eds. Retinal degenerations: Mechanisms and experimental therapy. New York: Kluwer Academic/Plenum Publishers, 2003.

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International Symposium on Retinal Degenerations (10th 2002 Bürgenstock, Switzerland). Retinal degenerations: Mechanisms and experimental therapy. New York: Kluwer Academic/Plenum Publishers, 2003.

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1941-, Shima Akihiro, ed. Frontiers of photobiology: Proceedings of the 11th International Congress on Photobiology, the 11th International Congress on Photobiology, Kyoto, Japan, 7-11 September 1992. Amsterdam: Excerpata Medica, 1993.

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Photoreceptor Cells Volume 15. Academic Press, 1993.

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Dartnall, Herbert J. A. Photochemistry of Vision. Springer London, Limited, 2012.

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(Editor), Matthew M. LaVail, Joe G. Hollyfield (Editor), and Robert E. Anderson (Editor), eds. Retinal Degenerations: Mechanisms and Experimental Therapy (Advances in Experimental Medicine and Biology). Springer, 2007.

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Book chapters on the topic "Retinal Cone Photoreceptor Cells"

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Carvalho, Livia S., and Luk H. Vandenberghe. "Understanding Cone Photoreceptor Cell Death in Achromatopsia." In Retinal Degenerative Diseases, 231–36. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_31.

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Ballios, Brian G., Saeed Khalili, Molly S. Shoichet, and Derek van der Kooy. "Induction of Rod and Cone Photoreceptor-Specific Progenitors from Stem Cells." In Retinal Degenerative Diseases, 551–55. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_90.

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Yau, K. W., and L. W. Haynes. "Gating Kinetics of the cGMP-Activated Conductance of Retinal Cones." In Signal Transduction in Photoreceptor Cells, 175–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76482-0_13.

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Mencl, Stine, Dragana Trifunović, Eberhart Zrenner, and François Paquet-Durand. "PKG-Dependent Cell Death in 661W Cone Photoreceptor-like Cell Cultures (Experimental Study)." In Retinal Degenerative Diseases, 511–17. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_63.

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Rapp, Matthew, Grace Woo, Muayyad R. Al-Ubaidi, S. Patricia Becerra, and Preeti Subramanian. "Pigment Epithelium-Derived Factor Protects Cone Photoreceptor-Derived 661W Cells from Light Damage Through Akt Activation." In Retinal Degenerative Diseases, 813–20. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_102.

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Kaplan, Henry J., Wei Wang, and Douglas C. Dean. "Restoration of Cone Photoreceptor Function in Retinitis Pigmentosa (RP): Retinal Cell-Based Therapy." In Stem Cell Biology and Regenerative Medicine, 157–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05222-5_9.

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Ma, Hongwei, and Xi-Qin Ding. "Thyroid Hormone Signaling and Cone Photoreceptor Viability." In Retinal Degenerative Diseases, 613–18. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_81.

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Chiang, Wei-Chieh Jerry, Heike Kroeger, Lulu Chea, and Jonathan H. Lin. "Pathomechanisms of ATF6-Associated Cone Photoreceptor Diseases." In Retinal Degenerative Diseases, 305–10. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_50.

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Minke, B., C. T. Rubinstein, I. Sahly, S. Bar-Nachum, E. Suss, J. Kleiman, T. Byk, and Z. Selinger. "The Molecular Mechanism of Retinal Degeneration in the Retinal Degeneration B (rdgB) Mutant of Drosophila." In Signal Transduction in Photoreceptor Cells, 281–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76482-0_20.

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Kolandaivelu, Saravanan, and Visvanathan Ramamurthy. "AIPL1 Protein and its Indispensable Role in Cone Photoreceptor Function and Survival." In Retinal Degenerative Diseases, 43–48. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_6.

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Conference papers on the topic "Retinal Cone Photoreceptor Cells"

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"Human retinal photoreceptor cells in glaucoma: destructive changes of mithochondria and mitophagy." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-302.

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Agrawal, Anant, Nikita Kedia, Zhuolin Liu, Ryan Sochol, and Daniel X. Hammer. "3D printed phantoms of retinal photoreceptor cells for evaluating adaptive optics imaging modalities." In Ophthalmic Technologies XXVIII, edited by Fabrice Manns, Per G. Söderberg, and Arthur Ho. SPIE, 2018. http://dx.doi.org/10.1117/12.2291759.

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Chen, Yiwei, Yi He, Jing Wang, Lina Xing, and Guohua Shi. "Automated unsupervised identification of cone photoreceptor cells in adaptive optics scanning laser ophthalmoscope images." In 2020 International Conference on Intelligent Computing and Human-Computer Interaction (ICHCI). IEEE, 2020. http://dx.doi.org/10.1109/ichci51889.2020.00049.

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Nasiatka, Patrick J., Michelle C. Hauer, Noelle R. B. Stiles, Jaw-Chyng Lue, Satsuki Takahashi, Rajat Agrawal, James D. Weiland, Mark S. Humayun, and Armand R. Tanguay. "An Intraocular Camera for Retinal Prostheses." In ASME 2007 2nd Frontiers in Biomedical Devices Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/biomed2007-38109.

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Abstract:
Blindness due to degenerative retinal diseases such as Retinitis Pigmentosa (RP) and Age-Related Macular Degeneration (AMD) afflict millions of people worldwide. Recent advances in retinal implants that bypass damaged photoreceptor cells and electrically stimulate the remaining healthy retinal neurons show promise for restoring functional vision to the blind [1]. Current intraocular retinal prostheses driven by an external camera mounted on the subject’s head require slow and unnatural head movements. To allow for normal foveation and expanded depth of field, a novel intraocular camera (IOC) has been designed to work in conjunction with an epiretinal microstimulator array, as shown schematically in Fig. 1.
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Lazareva, Anfisa, Panos Liatsis, and Franziska G. Rauscher. "An automated image processing system for the detection of photoreceptor cells in adaptive optics retinal images." In 2015 International Conference on Systems, Signals and Image Processing (IWSSIP). IEEE, 2015. http://dx.doi.org/10.1109/iwssip.2015.7314210.

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