Relevant bibliographies by topics / Retina

Academic literature on the topic 'Retina'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Retina"

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CAMERON, DAVID A. "Cellular proliferation and neurogenesis in the injured retina of adult zebrafish." Visual Neuroscience 17, no. 5 (September 2000): 789–97. http://dx.doi.org/10.1017/s0952523800175121.

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The retinas of adult teleost fish can regenerate neurons following a chemical or mechanical injury. Previous studies have demonstrated that mechanical excision of fish retina induces a hyperplasia within the retinal sheet, including the formation of a proliferative blastema from whence new retinal cells are produced to fill the excision site. The current study was designed to address two issues regarding injury-induced retinal hyperplasia: (1) Retinas of adult zebrafish can regenerate following a surgical excision, but compared to other fish they contain very few proliferative cells: Might retinal injury in adult zebrafish therefore induce minimal, or perhaps no, hyperplasia? (2) The fate of injury-induced, proliferative retinal cells outside surgical excision sites has yet to be determined. Do such cells produce retinal neurons? Evidence is presented that mechanical injury to the adult zebrafish retina induces a dramatic increase in the number of proliferative cells both within and external to the lesion site, and some of these cells apparently migrate within the radial dimension of the retina. Evidence is also presented that injury-induced proliferative cells outside a lesion site can produce retinal neurons—including cone photoreceptors, interplexiform cells, and amacrine cells—that are incorporated into the extant retina. The results suggest that the adult zebrafish retina contains a latent population of cells that is induced to proliferate following retinal injury, and that these cells might represent a novel avenue for pluripotent neurogenesis within the intact adult teleost retina.
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HANKINS, M. W. "Functional dopamine deficits in the senile rat retina." Visual Neuroscience 17, no. 6 (November 2000): 839–45. http://dx.doi.org/10.1017/s0952523800176035.

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The activity of the endogenous retinal dopamine (DA) pathway has been examined in the pigmented rat using retinas obtained from normal adult (∼3 months) and senile adults (∼24 months) using an in vitro electrophysiological approach. By comparing the pharmacological sensitivity of the horizontal cells (HCs) to exogenous DA, a D1 receptor antagonist (SCH 23390) and a DA-transport inhibitor (nomifensine), it is suggested that there is a functional deficit in the endogenous DA activity in the senile retina. Cells recorded from retinae obtained from senile animals are more sensitive to exogenous DA, whilst the senile retina is insensitive to SCH 23390. In addition, nomifensine was effective in potentiating subthreshold DA applications, but only in the normal adult retina. The data may suggest that endogenous DA release upon the HCs and selective re-uptake are suppressed in these retinae. These functional deficits also appear to be associated with changes in the receptive fields of the HCs, suggesting there is a corresponding deficit in spatial processing at the outer plexiform layer (OPL) of the senile rat.
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Acosta, Monica L., Michael Kalloniatis, and David L. Christie. "Creatine transporter localization in developing and adult retina: importance of creatine to retinal function." American Journal of Physiology-Cell Physiology 289, no. 4 (October 2005): C1015—C1023. http://dx.doi.org/10.1152/ajpcell.00137.2005.

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Creatine and phosphocreatine are required to maintain ATP needed for normal retinal function and development. The aim of the present study was to determine the distribution of the creatine transporter (CRT) to gain insight to how creatine is transported into the retina. An affinity-purified antibody raised against the CRT was applied to adult vertebrate retinas and to mouse retina during development. Confocal microscopy was used to identify the localization pattern as well as co-localization patterns with a range of retinal neurochemical markers. Strong labeling of the CRT was seen in the photoreceptor inner segments in all species studied and labeling of a variety of inner neuronal cells (amacrine, bipolar, and ganglion cells), the retinal nerve fibers and sites of creatine transport into the retina (retinal pigment epithelium, inner retinal blood vessels, and perivascular astrocytes). The CRT was not expressed in Müller cells of any of the species studied. The lack of labeling of Müller cells suggests that neurons are independent of this glial cell in accumulating creatine. During mouse retinal development, expression of the CRT progressively increased throughout the retina until approximately postnatal day 10, with a subsequent decrease. Comparison of the distribution patterns of the CRT in vascular and avascular vertebrate retinas and studies of the mouse retina during development indicate that creatine and phosphocreatine are important for ATP homeostasis.
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McPherson, Scott, Neal Heuss, Mark Pierson, and Dale Gregerson. "Analysis of CNS tissue-specific Tregs and dendritic cells in T cell responses and autoimmunity (MUC7P.757)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 197.9. http://dx.doi.org/10.4049/jimmunol.192.supp.197.9.

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Abstract We assessed locally generated, locally acting peripheral regulatory T cells (pTregs) in retinal immune homeostasis and ability of retinal dendritic cells (DC) to support T cell activation/expansion within retina. We used transgenic (Tg) mice expressing beta-galactosidase (bgal mice) as retinal neo-self antigen, TCR Tg mice (BG2) specific for bgal, and mice with labeled, depletable Tregs or DC, based on expression of diphtheria toxin (DTx) receptor and/or GFP controlled by FoxP3 or CD11c promoter (FDG or CDG mice). Treg and DC depletion from retina was done by DTx injection into the eye. T cells and DC were assayed by FACS of retina or blood. Retinal autoimmunity was assessed by histological analysis. After bgal (FDG/bgal mice) or IRBP (FDG mice) immunization, Treg depleted retinas showed increased incidence and severity of autoimmunity. We found local depletion of Tregs from retina sufficient to induce spontaneous autoimmunity in FDG/bgal/BG2 mice but not in single or double Tg mice. Dose of DTx used to eliminate retinal Tregs did not induce retinal autoimmunity if given systemically. DC depletion from the retina prevented Treg and Teff generation within retina after bgal injection. Retinal microglia remaining after DC depletion did not make up for the loss of DC-dependent antigen presentation. We conclude local Tregs within the retina protect against spontaneous organ-specific autoimmunity and local DC must be present within the retina for antigen presentation to T cells.
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Beach, Krista M., Jianbo Wang, and Deborah C. Otteson. "Regulation of Stem Cell Properties of Müller Glia by JAK/STAT and MAPK Signaling in the Mammalian Retina." Stem Cells International 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/1610691.

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In humans and other mammals, the neural retina does not spontaneously regenerate, and damage to the retina that kills retinal neurons results in permanent blindness. In contrast to embryonic stem cells, induced pluripotent stem cells, and embryonic/fetal retinal stem cells, Müller glia offer an intrinsic cellular source for regenerative strategies in the retina. Müller glia are radial glial cells within the retina that maintain retinal homeostasis, buffer ion flux associated with phototransduction, and form the blood/retinal barrier within the retina proper. In injured or degenerating retinas, Müller glia contribute to gliotic responses and scar formation but also show regenerative capabilities that vary across species. In the mammalian retina, regenerative responses achieved to date remain insufficient for potential clinical applications. Activation of JAK/STAT and MAPK signaling by CNTF, EGF, and FGFs can promote proliferation and modulate the glial/neurogenic switch. However, to achieve clinical relevance, additional intrinsic and extrinsic factors that restrict or promote regenerative responses of Müller glia in the mammalian retina must be identified. This review focuses on Müller glia and Müller glial-derived stem cells in the retina and phylogenetic differences among model vertebrate species and highlights some of the current progress towards understanding the cellular mechanisms regulating their regenerative response.
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Pfister, Delaney, Chuanjiang Yu, Da Som Kim, Jingling Li, Audrey Drewing, and Lei Li. "Zebrafish Olfacto-Retinal Centrifugal Axon Projection and Distribution: Effects of Gonadotropin-Releasing Hormone and Dopaminergic Signaling." Developmental Neuroscience 38, no. 1 (October 28, 2015): 27–33. http://dx.doi.org/10.1159/000439524.

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The terminalis neurons (TNs) have been described in teleost species. In zebrafish, the TNs are located in the olfactory bulb. The TNs synthesize and release gonadotropin-releasing hormone (GnRH) as one of the major neurotransmitters. The TNs project axons to many brain areas, which include the neural retina. In the retina, the TN axons synapse with dopaminergic interplexiform cells (DA-IPCs) and retinal ganglion cells (RGCs). In this research, we examine the role of GnRH and dopaminergic signaling in TN axon projection to the retina using the transgenic zebrafish Tg(GnRH-3::GFP). While the TNs developed at 34 h postfertilization (hpf), the first TN axons were not detected in the retina until 48-50 hpf, when the first DA-IPCs were differentiated. In developing embryos, inhibition of retinal GnRH signaling pathways severely interrupted the projection of TN axons to the retina. However, inhibition of retinal dopaminergic signaling produced little effect on TN axon projection. In adult retinas, inactivation of GnRH receptors disrupted the patterns of TN axon distribution, and depletion of DA-IPCs abolished the TN axons. When DA-IPCs regenerated, the TN axons reappeared. Together, the data suggest that in developing zebrafish retinas GnRH signaling is required for TN axon projection, whereas in adult retinas activation of GnRH and dopaminergic signaling transduction is required for normal distribution of the TN axons.
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Greco, Jordan A., Nicole L. Wagner, Ralph J. Jensen, Daniel B. Lawrence, Matthew J. Ranaghan, Megan N. Sandberg, Daniel J. Sandberg, and Robert R. Birge. "Activation of retinal ganglion cells using a biomimetic artificial retina." Journal of Neural Engineering 18, no. 6 (December 1, 2021): 066027. http://dx.doi.org/10.1088/1741-2552/ac395c.

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Abstract Objective. Biomimetic protein-based artificial retinas offer a new paradigm for restoring vision for patients blinded by retinal degeneration. Artificial retinas, comprised of an ion-permeable membrane and alternating layers of bacteriorhodopsin (BR) and a polycation binder, are assembled using layer-by-layer electrostatic adsorption. Upon light absorption, the oriented BR layers generate a unidirectional proton gradient. The main objective of this investigation is to demonstrate the ability of the ion-mediated subretinal artificial retina to activate retinal ganglion cells (RGCs) of degenerated retinal tissue. Approach. Ex vivo extracellular recording experiments with P23H line 1 rats are used to measure the response of RGCs following selective stimulation of our artificial retina using a pulsed light source. Single-unit recording is used to evaluate the efficiency and latency of activation, while a multielectrode array (MEA) is used to assess the spatial sensitivity of the artificial retina films. Main results. The activation efficiency of the artificial retina increases with increased incident light intensity and demonstrates an activation latency of ∼150 ms. The results suggest that the implant is most efficient with 200 BR layers and can stimulate the retina using light intensities comparable to indoor ambient light. Results from using an MEA show that activation is limited to the targeted receptive field. Significance. The results of this study establish potential effectiveness of using an ion-mediated artificial retina to restore vision for those with degenerative retinal diseases, including retinitis pigmentosa.
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Caminos, Elena, Susana López-López, and Juan R. Martinez-Galan. "Selective Assembly of TRPC Channels in the Rat Retina during Photoreceptor Degeneration." International Journal of Molecular Sciences 25, no. 13 (June 30, 2024): 7251. http://dx.doi.org/10.3390/ijms25137251.

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Transient receptor potential canonical (TRPC) channels are calcium channels with diverse expression profiles and physiological implications in the retina. Neurons and glial cells of rat retinas with photoreceptor degeneration caused by retinitis pigmentosa (RP) exhibit basal calcium levels that are above those detected in healthy retinas. Inner retinal cells are the last to degenerate and are responsible for maintaining the activity of the visual cortex, even after complete loss of photoreceptors. We considered the possibility that TRPC1 and TRPC5 channels might be associated with both the high calcium levels and the delay in inner retinal degeneration. TRPC1 is known to mediate protective effects in neurodegenerative processes while TRPC5 promotes cell death. In order to comprehend the implications of these channels in RP, the co-localization and subsequent physical interaction between TRPC1 and TRPC5 in healthy retina (Sprague-Dawley rats) and degenerating (P23H-1, a model of RP) retina were detected by immunofluorescence and proximity ligation assays. There was an overlapping signal in the innermost retina of all animals where TRPC1 and TRPC5 physically interacted. This interaction increased significantly as photoreceptor loss progressed. Both channels function as TRPC1/5 heteromers in the healthy and damaged retina, with a marked function of TRPC1 in response to retinal degenerative mechanisms. Furthermore, our findings support that TRPC5 channels also function in partnership with STIM1 in Müller and retinal ganglion cells. These results suggest that an increase in TRPC1/5 heteromers may contribute to the slowing of the degeneration of the inner retina during the outer retinal degeneration.
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Isayama, Tomoki, Patricia J. McLaughlin, and Ian S. Zagon. "Ontogeny of preproenkephalin mRNA expression in the rat retina." Visual Neuroscience 13, no. 4 (July 1996): 695–704. http://dx.doi.org/10.1017/s0952523800008580.

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AbstractEndogenous opioid systems (i.e. opioid peptides and opioid receptors) modulate developmental events in the neonatal mammalian retina. In the present study, the mRNA encoding preproenkephalin A (PPE), the prohormone for the opioid growth factor (OGF), [Met5]-enkephalin, was studied in the developing and the adult retinas of rats. Northern analysis indicated the presence of a 1.4-kb message in the developing and adult retinas corresponding to rat PPE mRNA. Quantitation showed that PPE message was present on postnatal day 1 at 5% of the adult level, and increased during development until the adult quantity was reached by postnatal day 27. In situ hybridization experiments first detected the presence of PPE mRNA in retinal tissues during late gestation. In late prenatal and neonatal retinas, PPE message was associated with areas of the developing retina containing proliferating neuroblasts and postmitotic cells. Later in development, message appeared to be located primarily within the inner retina, with abundant PPE mRNA associated with putative horizontal cells of the inner nuclear layer (INL). The adult retina showed a similar pattern of PPE gene expression in the cells of the INL. These findings document that the gene expression in the retina for PPE begins in the fetus, continues during retinal development, and coincides with the presence of a PPE mRNA derivative ([Met5]-enkephalin) that regulates DNA synthesis during retinal ontogeny. Our results are also the first to show the presence of PPE message in the adult mammalian retina, suggesting transcription of an opioid gene in the mature visual system.
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Wang, Shuyi, Xiuying Jiang, Weijia Peng, Shuangjian Yang, Rongbiao Pi, and Shiyou Zhou. "Acrolein Induces Retinal Abnormalities of Alzheimer’s Disease in Mice." International Journal of Molecular Sciences 24, no. 17 (September 1, 2023): 13576. http://dx.doi.org/10.3390/ijms241713576.

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It is reported that retinal abnormities are related to Alzheimer’s disease (AD) in patients and animal models. However, it is unclear whether the retinal abnormities appear in the mouse model of sporadic Alzheimer’s disease (sAD) induced by acrolein. We investigated the alterations of retinal function and structure, the levels of β-amyloid (Aβ) and phosphorylated Tau (p-Tau) in the retina, and the changes in the retinal vascular system in this mouse model. We demonstrated that the levels of Aβ and p-Tau were increased in the retinas of mice from the acrolein groups. Subsequently, a decreased amplitudes of b-waves in the scotopic and photopic electroretinogram (ERG), decreased thicknesses of the retinal nerve fiber layer (RNFL) in the retina, and slight retinal venous beading were found in the mice induced by acrolein. We propose that sAD mice induced by acrolein showed abnormalities in the retina, which may provide a valuable reference for the study of the retina in sAD.
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Dissertations / Theses on the topic "Retina"

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Ivert, Lena. "Interactions between neural retina, retinal epithelium and choroid /." Stockholm : Section of ophthalmology and vision, Department of clinical neuroscience, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-797-9/.

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Wu, Kathy H. "Histopathological studies of the aging human retina." Thesis, The University of Sydney, 2002. https://hdl.handle.net/2123/27837.

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Age-related macular degeneration (AMD) is the leading cause of untreatable blindness. Its global prevalence continues to increase in relation to aging of the population. Despite the increasing impact of AMD, its pathogenesis remains to be fully defined. Improved therapeutic measures such as photodynamic therapy and pharmacological interventions are being developed for some cases of Wet AMD; however, treatment remains unavailable for the Dry form which accounts for a significant proportion of AMD cases. Neither has any intervention been developed to reduce the incidence of the disease.
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Larsson, Jörgen. "Central retinal vein occlusion certain risk factors, electroretinography and an experimental treatment model /." Lund : Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945007.html.

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West, Heloise Joan. "Control of retinal astrocyte numbers during development of the retina." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405230.

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Cox, Orla T. "Vascular cell death in diabetic retinopathy." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343079.

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Усенко, Наталія Миколаївна, Наталия Николаевна Усенко, Nataliia Mykolaivna Usenko, and T. S. Starostenko. "Artificial retina." Thesis, Вид-во СумДУ, 2011. http://essuir.sumdu.edu.ua/handle/123456789/22108.

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Mellough, Carla Bernadette. "An assessment of the cell replacement capability of immortalised, clonal and primary neural tissues following their intravitreal transplantation into rodent models of selective retinal ganglion cell depletion." University of Western Australia. School of Anatomy and Human Biology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0101.

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[Truncated abstract] Microenvironmental changes associated with apoptotic neural degeneration may instruct a proportion of newly transplanted donor cells to differentiate towards the fate of the deteriorating host cellular phenotype. In the work described in this thesis, this hypothesis was tested by inducing apoptotic retinal ganglion cell (RGC) death in neonatal and adult rats and mice, and then examining whether intravitreally grafted cells from a range of sources of donor neural tissue became incorporated into these selectively depleted retinae. Donor tissues were: a postnatal murine cerebellar-derived immortalised neural precursor cell line (C17.2); an adult rat hippocampal-derived clonal stem-like line (HCN/GFP); mouse embryonic day 14 (E14) primary dissociated retinal cells (Gt[ROSA]26); and adult mouse ciliary pigmented margin-derived primary neurospheres (Gt[ROSA]26). In neonates, rapid RGC death was induced by removal of the contralateral superior colliculus (SC), and in adults, delayed RGC death was induced by unilateral optic nerve (ON) transection. Some adult hosts received ON transection coupled with an autologous peripheral nerve (PN) graft. Donor cells were injected intravitreally 6-48 h after SC ablation (neonates) or 0, 5, 7 or 14 days after ON injury (adults). Cells were also injected into non-RGC depleted neonatal and adult retinae. At 4 or 8 weeks, transplanted cells were identified, quantified and their differentiation fate within host retinae was assessed. Transplanted male C17.2 cells were identified in host retinae using a Y-chromosome marker and in situ hybridisation, or by their expression of the lacZ reporter gene product Escherichia coli beta-galactosidase (beta-gal) using Xgal histochemistry or a beta-gal antibody. No C17.2 cells were identified in axotomised adult-injected eyes undergoing delayed RGC apoptosis (n = 16). Donor cells were, however, stably integrated within the retina in 29% (15/55) of mice that received C17.2 cell injections 24 h after neonatal SC ablation; 6-31% of surviving cells were found in the RGC layer (GCL). These NSC-like cells were also present in intact retinae, but on average there were fewer cells in GCL. In SC-ablated mice, most grafted cells did not express retinal-specific markers, although occasional donor cells in the GCL were immunopositive for beta-III tubulin (TUJ1), a protein highly iii expressed by, but not specific to, developing RGCs. Targeted rapid RGC depletion thus increased C17.2 cell incorporation into the GCL, but grafted C17.2 cells did not appear to differentiate into an RGC phenotype.
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Allende, Marie Alexandra. "Blood vessel growth in primate retinal development relationship of retinal maturation with choriocapillaris growth and a role for TGF-ß in the retina /." Connect to full text, 2008. http://hdl.handle.net/2123/4145.

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Thesis (Ph. D.)--University of Sydney, 2008.
Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Department of Clinical Ophthalmology and Eye Health, Faculty of Medicine. Title from title screen (viewed Apr. 8, 2009) Includes bibliography. Also available in print form.
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Whiteley, Simon J. O. "Deterioration and repair of visual function in the Royal College of Surgeons rat." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.344049.

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Leonelli, Mauro. "Receptores vanilóides TRPV1 na retina." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-22072011-131242/.

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A expressão do receptor de potencial receptor transiente, vanilóide 1 (TRPV1) começa desde estágios pré-sinaptogênicos da retina. O bloqueio farmacológico desse receptor nesse período diminui a apoptose fisiológica, havendo possível envolvimento da sinalização de MAP quinases. Na retina do animal adulto, observamos que a expressão de TRPV1 é amplamente difundida, albergando neurônios, células endoteliais e células da microglia. A ativação dos receptores TRPV1 é potencialmente citotóxica, e os mecanismos que podem estar envolvidos incluem a liberação de glutamato, a excitotoxicidade e o estresse nitrosativo. Evidenciamos que a lesão prévia de células ganglionares sensibiliza o tecido retiniano à citotoxicidade mediada pela estimulação de TRPV1. Porém, o bloqueio de TRPV1, tanto in vivo quanto in vitro, não inibiu a morte de células ganglionares axotomizadas. Esses dados sugerem que o receptor TRPV1 participa da modulação de diversos processos fisiopatológicos na retina.
TRPV1 expression in the developing retina begins before retinal sinaptogenesis. TRPV1 blockade reduced the normal apoptosis in this period, and MAPK signaling seems to be involved in this process. In the adult retina, TRPV1 are expressed in neuronal, endothelial and microglial cells. The activation of those receptors is potentially cytotoxic, and glutamate release and further excitotoxicity and nitrosative stress might be also involved. Axotomized retinal ganglion cells were sensitized to TRPV1 citotoxicity, but TRPV1 antagonism, both in vitro and in vivo, did not reduce the loss of ganglion cell after axotomy. Our results suggest that TRPV1 receptors are involved in synaptic function and homeostatic control in the retina. Moreover, TRPV1 seems to be indirectly involved in cellular degeneration that follows the section of retinal ganglion cell axons.
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Books on the topic "Retina"

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Richard, Spaide, and SpringerLink (Online service), eds. Medical Retina: Focus on Retinal Imaging. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Wu, Gloria. Retina: The fundamentals. Philadelphia: W.B. Saunders, 1995.

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1940-, Ryan Stephen J., ed. Retina. 2nd ed. St. Louis: Mosby, 1994.

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1940-, Ryan Stephen J., ed. Retina. St. Louis: Mosby, 1989.

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J, Ryan Stephen, Schachat Andrew P, Murphy Robert B, and Patz Arnall, eds. Retina. St. Louis: Mosby, 1989.

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Hakim, Lokman. Retina. Petaling Jaya, Malaysia: Buku Fixi, 2014.

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C, Ho Allen, and Wills Eye Hospital (Philadelphia, Pa.), eds. Retina. New York: McGraw-Hill, Medical Pub. Division, 2003.

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J, Ryan Stephen, Ogden Thomas E, and Schachat Andrew P, eds. Retina. St. Louis: Mosby, 1989.

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1940-, Ryan Stephen J., ed. Retina. 4th ed. Philadelphia: Elsevier Mosby, 2006.

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1940-, Ryan Stephen J., ed. Retina. 3rd ed. St. Louis: Mosby, 2001.

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Book chapters on the topic "Retina"

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"Medical retina." In Oxford Handbook of Ophthalmology, edited by Alastair K. O. Denniston and Philip I. Murray, 568–661. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198804550.003.0013.

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‘Medical retina‘ provides the reader with a practical approach to the assessment and management of retinal disease. After outlining the relevant anatomy and physiology of this structure, the chapter addresses the key clinical presentations arising from retinal disease, notably age-related macular degeneration, diabetic eye disease, cystoid macular oedema, retinal vascular disease, and genetic retinal disease. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition.
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Denniston, Alastair K. O., and Philip I. Murray. "Medical retina." In Oxford Handbook of Ophthalmology, 515–92. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199679980.003.0013.

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‘Medical retina’ provides the reader with a practical approach to the assessment and management of retinal disease. After outlining the relevant anatomy and physiology of this structure, the chapter addresses the key clinical presentations arising from retinal disease, notably age-related macular degeneration, diabetic eye disease, cystoid macular oedema, retinal vascular disease, and genetic retinal disease. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition.
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"Copyright." In Retina, iv. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50001-3.

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Macsai, Marian S., and Jay S. Duker. "Series Preface." In Retina, ix. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50002-5.

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Rogers, Adam H. "Preface." In Retina, x. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50003-7.

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Rogers, Adam H. "Dedication." In Retina, xi. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50004-9.

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Rogers, Adam H., and Jay S. Duker. "Diabetes." In Retina, 1–11. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50005-0.

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Rogers, Adam H., and Jay S. Duker. "Age-related Macular Degeneration." In Retina, 13–29. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50006-2.

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Rogers, Adam H., and Jay S. Duker. "Vascular Obstructions." In Retina, 31–73. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50007-4.

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Rogers, Adam H., and Jay S. Duker. "Pediatric." In Retina, 75–83. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-323-04959-7.50008-6.

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Conference papers on the topic "Retina"

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Packer, Orin, Christine A. Curcio, and Anita E. Hendrickson. "Asymmetric photoreceptor topography in the pigtail macaque (Macaca nemestrina) retina." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.fj1.

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Asymmetries in the distribution of photoreceptor size, density, and packing order have important consequences for the intepretation of anatomic models of retinal development and models of visual function that make assumptions about the geometry of the photoreceptor mosaic. Cone density and inner segment diameter were measured in whole mounted, nondehydrated pigtail macaque (Macaca nemestrina) retinas, viewed under Nomarski optics. Highest cone densities in the foveal center of two adult animals averaged 189,000 cones/mm2. Along the horizontal meridian, there were more cones at equal eccentricities in the peripheral nasal retina than in the peripheral temporal retina. The nasotemporal ratio increased with eccentricity, reaching a maximum of 3:1. On the vertical meridian, the inferior retina was higher in density than the superior retina by a maximum ratio of 1.5:1. Cone inner segment diameter in one animal ranged from 2.6 μm at the foveal center to over 11 μm in the periphery, in all retinal quadrants. Since cones at comparable eccentricities in nasal and temporal retina have equal diameters, the proportion of peripheral retina covered by cones is greater nasally than temporally.
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Curcio, Christine A. "Diameters of presumed cone apertures in human retina." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/oam.1987.wl1.

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The cone entrance aperture is thought to be located in the inner segment. Little is known about changes in cone inner segment diameter (CISD) across the entire human retina. The degree to which the increase in CISD with eccentricity offsets decline in cone density to maintain total quantal flux per unit retinal area is unknown. Gradients in refractive index along the length of CIS were viewed directly in cleared retinal whole mounts using Normarski differential interference contrast microscopy. Individual CISs are optically resolvable from their neighbors at a level slightly vitreal to the CIS ellipsoid–myoid junction. CISD at this presumed aperture level and the proportion of retinal area occupied by apertures aa were measured from the fovea of one and the periphery of four young adult retinas previously mapped for cone density. CISD increased sharply from 2.3 μm at the foveal center to 6.5 μm at 1 mm (3.6°) and slowly from there to a maximum of 8.5–9 μm near the ora serrata. aa decreased approximately threefold across the retina from 69 to 78% in the foveola to a plateau of 20–35% in the midperiphery to far periphery. Over this eccentricity range, the cone density declined fortyfold. These results predict different eccentricity dependencies for visual functions explained by the density of cones and those explained by the number of photons available to cone photopigment.
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Troilo, David. "Changes in Retinal Morphology following Experimentally Induced Myopia." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/vsia.1998.suc.4.

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The effects of increased eye size on retinal cell topography and morphology were examined using experimental animal models of myopia (chick and marmoset). Retinas from experimentally enlarged eyes have significantly larger areas than control eyes. Changes in the topography of cell density and the morphological structure of dendritic arbors of cells in the inner retina are consistent with the hypothesis that the retina stretches as the eye grows. In the marmoset, experimentally enlarged eyes had higher foveal cone densities than controls suggesting that stretch is an important factor in the increasing photoreceptor packing observed during normal foveal development. The increased axial length, retinal magnification, and foveal photoreceptor packing in experimental myopia suggest that the potential for higher acuity vision exists in human myopes. Any observed limitations in the acuity in myopes may result from other causes.
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Fitzke, F. W., G. Timberlake, W. H. Woon, J. Marshall, and A. C. Bird. "Optical modifications to a scanning laser ophthalmoscope for high-magnification, narrow optical section imaging." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.mpp8.

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A lens system was designed and incorporated into a prototype Rodenstock scanninglaser ophthalmoscope, which provided additional magnification of retinal structures and further narrowing of optical sections. The lens system increased the effective numerical aperture of the eye. In addition, smaller pinholes were used for the confocal aperture. The optical-section thickness was measured by using an artificial eye and positioning an artificial retina near the plane of focus under micrometer control. The digitized images were averaged over a central area of 16 × 16 pixels, and intensity was measured as a function of "retinal" position. The results showed that sections with half-widths < 70μm could be achieved. An infrared diodelaser was used to image the living human retina with this system. The maximum retinal irradiance was calculated to be within the standards of the American National Standards Institute. High-magnification images of the retina were acquired at different section depths. These results suggest that it is possible to image the microscopic structure of the living human retina. This may be useful in characterizing and studying microanatomical and functional alterations (measured by high-resolution SLO perimetry) in the human retina.
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Raghavi, K., Ranjith Balakrishnan, and J. S. Leena Jasmine. "Detecting retina artifacts from retin opthalmoscope scanning images based on retinal area detector." In 2016 International Conference on Communication and Signal Processing (ICCSP). IEEE, 2016. http://dx.doi.org/10.1109/iccsp.2016.7754430.

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Feng, Guanping, Karteek Kunala, Qiang Yang, and Jesse Schallek. "Adaptive optics 3D phase-contrast retinal imaging." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/fio.2022.fw6d.1.

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Illuminating the retina with a point-scan system, we measured angle-resolved light that returns from the retina to render 3D phase-contrast and plenoptic imaging of various retinal cells and structures.
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Rusovici, R., D. Dalli, K. Mitra, M. Calhoun, R. Mazzocchi, and M. Grace. "Design of Retinal Stent Using Finite Element Analysis." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14477.

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The retina is a light-sensitive tissue layer that lines the inside of the eye and relays visual information directly to the brain via the optic nerve. Retinal detachment occurs when the retina is lifted or pulled from its physiological location. This condition can result in partial or total vision loss. Retinal detachmentis a leading cause of permanent vision loss.
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MacLeod, Donald I. A. "Analysis of the Stiles-Crawford effect: the visual effects of cone acceptance angle, cone disarray, and retinal scatter." In Ophthalmic and Visual Optics. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/ovo.1993.osaa.3.

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The directional sensitivity of the retina is the joint result of many interacting factors, including the angular tuning of individual cones, the variation in tilt among different cones, and the scattering of light in the inner layers of the retina en route to the cones. Cone disarray and retinal scatter degrade the absolute sensitivity of the retina as well as broadening the Stiles-Crawford effect. Optical and psycho-physical sources of evidence are reviewed which suggest that retinal scatter and cone disarray, though measurable and functionally significant in many contexts, are not sufficient to make the normal distribution of visual sensitivity over the pupil much broader than is implied by the angular tuning of individual cones.
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Murphy, Christian, Gail Kaiser, Kristin Loveland, and Sahar Hasan. "Retina." In the 40th ACM technical symposium. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1508865.1508929.

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Wan, Gerry, Fengchen Gong, Tom Barbette, and Zakir Durumeric. "Retina." In SIGCOMM '22: ACM SIGCOMM 2022 Conference. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3544216.3544227.

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Reports on the topic "Retina"

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Nitta, Carolina, Jerilyn A. Timlin, and Michael B. Sinclair. Analysis of Fixed Retina Samples. Office of Scientific and Technical Information (OSTI), July 2014. http://dx.doi.org/10.2172/1171445.

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Beckerman, M. Modeling and Simulation of Microelectrode-Retina Interactions. Office of Scientific and Technical Information (OSTI), November 2002. http://dx.doi.org/10.2172/810944.

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Lazzi, Gianluca. Artificial Retina Project: Electromagnetic and Thermal Effects. Office of Scientific and Technical Information (OSTI), August 2014. http://dx.doi.org/10.2172/1150817.

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CONCEPTUAL MINDWORKS INC SAN ANTONIO TX. Simulating the Effects of Laser Damage to the Retina. Fort Belvoir, VA: Defense Technical Information Center, December 2001. http://dx.doi.org/10.21236/ada398963.

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de la Rosa, Enrique. Las distrofias hereditarias de la retina: un doble reto. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), December 2014. http://dx.doi.org/10.18567/sebbmdiv_anc.2014.12.1.

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Timlin, Jerilyn A., Thomas Edwin Beechem, Anthony E. McDonald, Matt Toomey, and Joseph Corbo. Raman Spectroscopy of HPLC Fractions from Retina Oil Droplets. Office of Scientific and Technical Information (OSTI), May 2014. http://dx.doi.org/10.2172/1531334.

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Hogren, Sarah. The Effects of Covid-19 on the Human Retina. Ames (Iowa): Iowa State University, May 2022. http://dx.doi.org/10.31274/cc-20240624-1427.

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Greenbaum, E., and J. Little. Artificial Retina Project: Final Report for CRADA ORNL 01-0625. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1023749.

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Willemsen, Jorge F. Feasibility Assessment of a Transient Sound Sensor Based on the Silicon Retina Architecture. Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada252288.

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Research, Gratis. Green Light: A New Preventive Therapy for Migraine. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.03.

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Manipulating the ability of green light to create the least amount of electrical signals in retina and brain cortex, green light therapy offers an excellent therapeutic role in reducing migraine pain and improves the quality of life
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