Journal articles on the topic 'Retina'
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1
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.
Full textAbstract:
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.
Full textAbstract:
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.
Full textAbstract:
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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Kartamihardja, Wedi Iskandar, Gilang Mutiara, Yanuar Zulkifli Harun, Maulya Listrianti, Bestari Yuniah, and Mayasari Kuntoyo. "Risk factors of immature retina on the first screening for retinopathy of prematurity." Paediatrica Indonesiana 63, no. 3 (June 30, 2023): 189–94. http://dx.doi.org/10.14238/pi63.3.2023.189-94.
Full textAbstract:
Background Immature retina is characterized by peripheral retinal avascularity. Retinal development is influenced by risk factors that affect retinal maturity.
Objective To identify risk factors for immature retina on the first retinopathy of prematurity (ROP) screening at the Neonatology Care Unit, Al-Islam Hospital, Bandung, in 2013-2021.
Methods This case-control, retrospective, observational study was performed by evaluating medical records of preterm infants screened for ROP. The subjects were divided into two groups, immature retina and mature retina. We recorded potential risk factors including gestational age (GA), birth weight (BW), birth weight for gestational age, respiratory distress syndrome (RDS), oxygen therapy >7 days, asphyxia, sepsis, multiple transfusion, apnea of prematurity (AOP), patent ductus arteriosus (PDA), and bronchopulmonary dysplasia (BPD) and analyzed them for potential associations with retinal development.
Results On the first ROP screening of 203 premature infants, 5 (2.5%) had ROP, 90 (44.6%) had immature retinas, and 107 (53.0%) had mature retinas. Bivariate logistic regression analysis showed significant relationships between immature retina (P<0.05), GA (OR=0.575; P=0.000), BW (OR=0.997; P=<0.001), gestational age maturity (OR=2.639; P=0.006), RDS (OR=1.809; P=0.042), oxygen therapy of >7 days (OR=4.494; P=0.002), sepsis (OR=2.028; P=0.034), multiple transfusions (OR=4.656; P=0.000), AOP (OR=2.553; P=0.002), PDA (OR=2.119; P=0.030). Multivariate regression analysis revealed a significant simultaneous relationship between all the risk factors and immature retina, with a Nägelkerke R2 value of 0.421.
Conclusion GA, BW, gestational age maturity, oxygen therapy of >7 days, sepsis, multiple transfusions, AOP, and PDA are significant risk factors of immature retina, be it independently or simultaneously.
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El-Darzi, Nicole, Natalia Mast, Brian Dailey, John Denker, Yong Li, Joseph Vance, and Irina A. Pikuleva. "Characterizations of Hamster Retina as a Model for Studies of Retinal Cholesterol Homeostasis." Biology 10, no. 10 (October 6, 2021): 1003. http://dx.doi.org/10.3390/biology10101003.
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Cholesterol homeostasis in the retina, a sensory organ in the back of the eye, has been studied in mice but not hamsters, despite the latter being more similar to humans than mice with respect to their whole-body cholesterol maintenance. The goal of this study was to begin to assess hamster retina and conduct initial interspecies comparisons. First, young (3-month old) and mature (6-month old) Syrian (golden) hamsters were compared with 3- and 6-month old mice for ocular biometrics and retinal appearance on optical coherence tomography and fluorescein angiography. Of the 30 evaluated hamsters, seven had retinal structural abnormalities and all had increased permeability of retinal blood vessels. However, hamsters did not carry the mutations causing retinal degenerations 1 and 8, had normal blood glucose levels, and only slightly elevated hemoglobin A1c content. Cholesterol and six other sterols were quantified in hamster retina and compared with sterol profiles in mouse and human retina. These comparisons suggested that cholesterol turnover is much higher in younger than mature hamster retina, and that mature hamster and human retinas share similarities in the ratios of cholesterol metabolites to cholesterol. This study supports further investigations of cholesterol maintenance in hamster retina.
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Wu, Sih-Rong, and Huda Y. Zoghbi. "TheAtoh1-CreKnock-In Allele Ectopically Labels a Subpopulation of Amacrine Cells and Bipolar Cells in Mouse Retina." eneuro 10, no. 11 (November 2023): ENEURO.0307–23.2023. http://dx.doi.org/10.1523/eneuro.0307-23.2023.
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AbstractThe retina has diverse neuronal cell types derived from a common pool of retinal progenitors. Many molecular drivers, mostly transcription factors, have been identified to promote different cell fates. InDrosophila,atonalis required for specifying photoreceptors. In mice, there are two closely relatedatonalhomologs,Atoh1andAtoh7. WhileAtoh7is known to promote the genesis of retinal ganglion cells, there is no study on the function ofAtoh1in retinal development. Here, we crossedAtoh1Cre/+mice to mice carrying a Cre-dependent TdTomato reporter to track potentialAtoh1-lineage neurons in retinas. We characterized a heterogeneous group of TdTomato+retinal neurons that were detected at the postnatal stage, including glutamatergic amacrine cells, AII amacrine cells, and BC3b bipolar cells. Unexpectedly, we did not observe TdTomato+retinal neurons in the mice with anAtoh1-FlpOknock-in allele and a Flp-dependent TdTomato reporter, suggestingAtoh1is not expressed in the mouse retina. Consistent with these data, conditional removal ofAtoh1in the retina did not cause any observable phenotypes. Importantly, we did not detectAtoh1expression in the retina at multiple ages using mice withAtoh1-GFPknock-in allele. Therefore, we conclude thatAtoh1Cre/+mice have ectopic Cre expression in the retina and thatAtoh1is not required for retinal development.
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LIANG, LI, YOSHIAKI KATAGIRI, LUISA M. FRANCO, YASUYUKI YAMAUCHI, VOLKER ENZMANN, HENRY J. KAPLAN, and JULIE H. SANDELL. "Long-term cellular and regional specificity of the photoreceptor toxin, iodoacetic acid (IAA), in the rabbit retina." Visual Neuroscience 25, no. 2 (March 2008): 167–77. http://dx.doi.org/10.1017/s0952523808080401.
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AbstractThis study investigated the anatomical consequences of a photoreceptor toxin, iodoacetic acid (IAA), in the rabbit retina. Retinae were examined 2 weeks, 1, 3, and 6 months after systemic IAA injection. The retinae were processed using standard histological methods to assess the gross morphology and topographical distribution of damage, and by immunohistochemistry to examine specific cell populations in the retina. Degeneration was restricted to the photoreceptors and was most common in the ventral retina and visual streak. In damaged regions, the outer nuclear layer was reduced in thickness or eliminated entirely, with a concomitant loss of immunoreactivity for rhodopsin. However, the magnitude of the effect varied between animals with the same IAA dose and survival time, suggesting individual differences in the bioavailability of the toxin. In all eyes, the inner retina remained intact, as judged by the thickness of the inner nuclear layer, and by the pattern of immunoreactivity for protein kinase C-α (rod bipolar cells) and calbindin D-28 (horizontal cells). Müller cell stalks became immunoreactive for glial fibrillary acidic protein (GFAP) even in IAA-treated retinae that had no signs of cell loss, indicating a response of the retina to the toxin. However, no marked hypertrophy or proliferation of Müller cells was observed with either GFAP or vimentin immunohistochemistry. Thus the selective, long lasting damage to the photoreceptors produced by this toxin did not lead to a reorganization of the surviving cells, at least with survival as long as 6 months, in contrast to the remodeling of the inner retina that is observed in inherited retinal degenerations such as retinitis pigmentosa and retinal injuries such as retinal detachment.
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Zhao, Shulei, Fang-Cheng Hung, Jennifer S. Colvin, Andrew White, Weilie Dai, Frank J. Lovicu, David M. Ornitz, and Paul A. Overbeek. "Patterning the optic neuroepithelium by FGF signaling and Ras activation." Development 128, no. 24 (December 15, 2001): 5051–60. http://dx.doi.org/10.1242/dev.128.24.5051.
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During vertebrate embryogenesis, the neuroectoderm differentiates into neural tissues and also into non-neural tissues such as the choroid plexus in the brain and the retinal pigment epithelium in the eye. The molecular mechanisms that pattern neural and non-neural tissues within the neuroectoderm remain unknown. We report that FGF9 is normally expressed in the distal region of the optic vesicle that is destined to become the neural retina, suggesting a role in neural patterning in the optic neuroepithelium. Ectopic expression of FGF9 in the proximal region of the optic vesicle extends neural differentiation into the presumptive retinal pigment epithelium, resulting in a duplicate neural retina in transgenic mice. Ectopic expression of constitutively active Ras is also sufficient to convert the retinal pigment epithelium to neural retina, suggesting that Ras-mediated signaling may be involved in neural differentiation in the immature optic vesicle. The original and the duplicate neural retinae differentiate and laminate with mirror-image polarity in the absence of an RPE, suggesting that the program of neuronal differentiation in the retina is autonomously regulated. In mouse embryos lacking FGF9, the retinal pigment epithelium extends into the presumptive neural retina, indicating a role of FGF9 in defining the boundary of the neural retina.
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Troilo, David, Meijuan Xiong, Justin C. Crowley, and Barbara L. Finlay. "Factors controlling the dendritic arborization of retinal ganglion cells." Visual Neuroscience 13, no. 4 (July 1996): 721–33. http://dx.doi.org/10.1017/s0952523800008609.
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AbstractThe effects of changing retinal ganglion cell (RGC) density and availability of presynaptic sites on the development of RGC dendritic arbor in the developing chick retina were contrasted. Visual form deprivation was used to induce ocular enlargement and expanded retinal area resulting in a 20–30% decrease in RGC density. In these retinas, RGC dendritic arbors increased in a compensatory manner to maintain the inner nuclear layer to RGC convergence ratio in a way that is consistent with simple stretching; RGC dendritic arbors become larger with increased branch lengths, but without change in the total number of branches. In the second manipulation, partial optic nerve section was used to produce areas of RGC depletion of approximately 60% in the central retina. This reduction in density is comparable to the density of locations in the normal peripheral retina. In RGC-depleted retinas, dendritic arbor areas of RGCs in the central retina grow to match the size of normal peripheral arbors. In contrast to the expanded case, two measures of intrinsic arbor structure are changed in RGC-depleted retinas; the branch density of RGC dendrites is greater, and the relative areas of the two arbors of bistratified cells are altered. We discuss the potential roles of retinal growth, local RGC density, and availability of presynaptic terminals in the developmental control of RGC dendritic arbor.
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Rodriguez, K. A., and A. T. Tsin. "Retinyl esters in the vertebrate neuroretina." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 1 (January 1, 1989): R255—R258. http://dx.doi.org/10.1152/ajpregu.1989.256.1.r255.
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High-performance liquid chromatography (HPLC) was employed to measure retinyl esters in the vertebrate retina. Both retina and retinal pigment epithelium (RPE) from frog, chicken, and bovine eyes were studied. In comparison to the RPE, the retina possessed a significant level of 11-cis and all trans retinyl palmitate. Using a sensitive radioassay, we also detected the presence of retinyl ester hydrolase (REH) activity in homogenates prepared from both retina and RPE. The rate of retinyl ester hydrolysis in these retinas was sufficiently high to supply retinal chromophores for the metabolic renewal and for the regeneration of visual pigments. In comparison to retinyl esters in the RPE, retinyl esters in the retina are located much closer to the sites of visual pigment synthesis and regeneration. Hence it is possible that these retinyl esters play a more important role in the visual cycle than those in the RPE.
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Chen, Jingfei, Qihui Luo, Chao Huang, Wen Zeng, Ping Chen, Qi Gao, Bing Chen, Wentao Liu, Lingzhen Pan, and Zhengli Chen. "Morphology of Inner Retina in Rhesus Monkeys of Various Ages: A Comparative Study." Journal of Ophthalmology 2019 (March 3, 2019): 1–7. http://dx.doi.org/10.1155/2019/7089342.
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Purpose. To investigate the changes of thickness in each layer, the morphology and density of inner neurons in rhesus monkeys’ retina at various growth stages, thus contribute useful data for further biological studies. Methods. The thickness of nerve fiber layer (NFL), the whole retina, inner plexiform layer (IPL), and outer plexiform layer (OPL) of rhesus monkeys at different ages were observed with hematoxylin and eosin (H&E) staining. The morphology and the density of inner neurons of rhesus monkey retina were detected by immunofluorescence. Results. The retina showed the well-known ten layers, the thickness of each retinal layer in rhesus monkeys at various ages increased rapidly after infant, and the retina was the thickest in adulthood, but the retinal thickness stop growing in senescent. Quantitative analysis showed that the maximum density of inner neurons was reached in adolescent, and then, the density of inner neurons decreased in adults and senescent retinas. And some changes in the morphology of rod bipolar cells have occurred in senescent. Conclusions. The structure of retina in rhesus monkeys is relatively immature at infant, and the inner retina of rhesus monkeys is mature in adolescent, while the thickness of each retinal layer was the most developed in the adult group. There was no significant change in senescence for the thickness of each retinal layer, but the number of the neurons in our study has a decreasing trend and the morphological structure has changed.
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Hyer, J., T. Mima, and T. Mikawa. "FGF1 patterns the optic vesicle by directing the placement of the neural retina domain." Development 125, no. 5 (March 1, 1998): 869–77. http://dx.doi.org/10.1242/dev.125.5.869.
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Patterning of the bipotential retinal primordia (the optic vesicles) into neural retina and retinal pigmented epithelium depends on its interaction with overlaying surface ectoderm. The surface ectoderm expresses FGFs and the optic vesicles express FGF receptors. Previous FGF-expression data and in vitro analyses support the hypothesis that FGF signaling plays a significant role in patterning the optic vesicle. To test this hypothesis in vivo we removed surface ectoderm, a rich source of FGFs. This ablation generated retinas in which neural and pigmented cell phenotypes were co-mingled. Two in vivo protocols were used to replace FGF secretion by surface ectoderm: (1) implantation of FGF-secreting fibroblasts, and (2) injection of replication-incompetent FGF retroviral expression vectors. The retinas in such embryos exhibited segregated neural and pigmented epithelial domains. The neural retina domains were always close to a source of FGF secretion. These results indicate that, in the absense of surface ectoderm, cells of the optic vesicles display both neural and pigmented retinal phenotypes, and that positional cues provided by FGF organize the bipotential optic vesicle into specific neural retina and pigmented epithelium domains. We conclude that FGF can mimic one of the earliest functions of surface ectoderm during eye development, namely the demarcation of neural retina from pigmented epithelium.
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Schilardi, Giulia, Jakub Kralik, and Sonja Kleinlogel. "Selective Block of Upregulated Kv1.3 Potassium Channels in ON-Bipolar Cells of the Blind Retina Enhances Optogenetically Restored Signaling." International Journal of Molecular Sciences 24, no. 18 (September 18, 2023): 14207. http://dx.doi.org/10.3390/ijms241814207.
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Loss of photoreceptors in retinal degenerative diseases also impacts the inner retina: bipolar cell dendrites retract, neurons rewire, and protein expression changes. ON-bipolar cells (OBCs) represent an attractive target for optogenetic vision restoration. However, the above-described maladaptations may negatively impact the quality of restored vision. To investigate this question, we employed human post-mortem retinas and transgenic rd1_Opto-mGluR6 mice expressing the optogenetic construct Opto-mGluR6 in OBCs and carrying the retinal degeneration rd1 mutation. We found significant changes in delayed rectifier potassium channel expression in OBCs of degenerative retinas. In particular, we found an increase in Kv1.3 expression already in early stages of degeneration. Immunohistochemistry localized Kv1.3 channels specifically to OBC axons. In whole-cell patch-clamp experiments, OBCs in the degenerated murine retina were less responsive, which could be reversed by application of the specific Kv1.3 antagonist Psora-4. Notably, Kv1.3 block significantly increased the amplitude and kinetics of Opto-mGluR6-mediated light responses in OBCs of the blind retina and increased the signal-to-noise ratio of light-triggered responses in retinal ganglion cells. We propose that reduction in Kv1.3 activity in the degenerated retina, either by pharmacological block or by KCNA3 gene silencing, could improve the quality of restored vision.
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Quinn, Peter M., Aat A. Mulder, C. Henrique Alves, Mélissa Desrosiers, Sharon I. de Vries, Jan Klooster, Deniz Dalkara, Abraham J. Koster, Carolina R. Jost, and Jan Wijnholds. "Loss of CRB2 in Müller glial cells modifies a CRB1-associated retinitis pigmentosa phenotype into a Leber congenital amaurosis phenotype." Human Molecular Genetics 28, no. 1 (September 19, 2018): 105–23. http://dx.doi.org/10.1093/hmg/ddy337.
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Abstract Variations in the human Crumbs homolog-1 (CRB1) gene lead to an array of retinal dystrophies including early onset of retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA) in children. To investigate the physiological roles of CRB1 and CRB2 in retinal Müller glial cells (MGCs), we analysed mouse retinas lacking both proteins in MGC. The peripheral retina showed a faster progression of dystrophy than the central retina. The central retina showed retinal folds, disruptions at the outer limiting membrane, protrusion of photoreceptor nuclei into the inner and outer segment layers and ingression of photoreceptor nuclei into the photoreceptor synaptic layer. The peripheral retina showed a complete loss of the photoreceptor synapse layer, intermingling of photoreceptor nuclei within the inner nuclear layer and ectopic photoreceptor cells in the ganglion cell layer. Electroretinography showed severe attenuation of the scotopic a-wave at 1 month of age with responses below detection levels at 3 months of age. The double knockout mouse retinas mimicked a phenotype equivalent to a clinical LCA phenotype due to loss of CRB1. Localization of CRB1 and CRB2 in non-human primate (NHP) retinas was analyzed at the ultrastructural level. We found that NHP CRB1 and CRB2 proteins localized to the subapical region adjacent to adherens junctions at the outer limiting membrane in MGC and photoreceptors. Our data suggest that loss of CRB2 in MGC aggravates the CRB1-associated RP-like phenotype towards an LCA-like phenotype.
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Shirai, Hiroshi, Michiko Mandai, Keizo Matsushita, Atsushi Kuwahara, Shigenobu Yonemura, Tokushige Nakano, Juthaporn Assawachananont, et al. "Transplantation of human embryonic stem cell-derived retinal tissue in two primate models of retinal degeneration." Proceedings of the National Academy of Sciences 113, no. 1 (December 22, 2015): E81—E90. http://dx.doi.org/10.1073/pnas.1512590113.
Full textAbstract:
Retinal transplantation therapy for retinitis pigmentosa is increasingly of interest due to accumulating evidence of transplantation efficacy from animal studies and development of techniques for the differentiation of human embryonic stem cells (hESCs) and induced pluripotent stem cells into retinal tissues or cells. In this study, we aimed to assess the potential clinical utility of hESC-derived retinal tissues (hESC-retina) using newly developed primate models of retinal degeneration to obtain preparatory information regarding the potential clinical utility of these hESC-retinas in transplantation therapy. hESC-retinas were first transplanted subretinally into nude rats with or without retinal degeneration to confirm their competency as a graft to mature to form highly specified outer segment structure and to integrate after transplantation. Two focal selective photoreceptor degeneration models were then developed in monkeys by subretinal injection of cobalt chloride or 577-nm optically pumped semiconductor laser photocoagulation. The utility of the developed models and a practicality of visual acuity test developed for monkeys were evaluated. Finally, feasibility of hESC-retina transplantation was assessed in the developed monkey models under practical surgical procedure and postoperational examinations. Grafted hESC-retina was observed differentiating into a range of retinal cell types, including rod and cone photoreceptors that developed structured outer nuclear layers after transplantation. Further, immunohistochemical analyses suggested the formation of host–graft synaptic connections. The findings of this study demonstrate the clinical feasibility of hESC-retina transplantation and provide the practical tools for the optimization of transplantation strategies for future clinical applications.
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del Cerro, Manuel, Mary F. D. Notter, Coca del Cerro, Stanley J. Wiegand, Donald A. Grover, and Eliot Lazar. "Intraretinal Transplantation for Rod-Cell Replacement in Light-Damaged Retinas." Journal of Neural Transplantation 1, no. 1 (1989): 1–10. http://dx.doi.org/10.1155/np.1989.1.
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Blindness from retinal disease is often the consequence of extensive damage to the photoreceptor cell population, while other cell types which form the neural retina are relatively spared. In this setting, transplantation of photoreceptor cells could offer hope for the restoration of some degree of visual function. We testd the feasibility of this approach by transplanting immature retinal cells into the eyes of adult rats affected by late stage phototoxic retinopathy, which are almost totally devoid of photoreceptor cells.Dissociated neuroretinal cells from newborn rats were injected into the hosts' retinas. These cells were labelled with the fluorescent tracer Fast-blue for identification within the host eye. Survival time ranged from 3 to 100 post-transplantation days.Fundus examination of light-irradiated eyes showed pallor caused by a considerable reduction of the retino-choroidal vascular bed after light irradiation. Histologically the hosts exhibited decimation of the elements forming the outer layers.throughout the entire retina.As visualized by light and electron microscopic procedures, we report the differentiation of clusters of transplanted photoreceptor cells, and the integration of these cells within the adjacent areas of the host retina.Fluorescence microscopy showed these clusters to be formed by fluorescently labelled cells developing in intimate contact with the unlabelled host retina. Electron microscopically it was possible to determine that these photoreceptors had established synaptic contacts. These observations indicate that successful transplantation of immature retinal cells is feasible into adult eyes that have suffered extensive retino-choroidal damage. These findings also support the concept that retinal transplantation is a procedure which may open new avenues into the study of retinal repair.
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Chen, Xiuping, Xianglian Li, Yan Liu, Yuanzhi Yuan, Yifan Feng, Jing Wang, Min Li, Dongmei Gao, and Fei Yuan. "MicroRNA Expression Analysis of Mice Retinas with Oxygen-Induced Retinopathy by RNA Sequencing." Journal of Ophthalmology 2022 (March 3, 2022): 1–9. http://dx.doi.org/10.1155/2022/9738068.
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Purpose. To characterize the microRNA (miRNA) expression profiles in the retinas of mice with oxygen-induced retinopathy by RNA sequencing and to ascertain miRNAs associated with retinal neovascularization. Methods. Retina samples were obtained from 3 groups (6 retinas/group) of OIR mice and normal mice at P17. RNA was isolated from 24 retina samples and then detected on an Illumina HiSeq. Twelve retina samples were used for quantitative polymerase chain reaction to validate the RNA sequencing. Bioinformatics analyses were performed. Result. The RNA sequence showed that 565 miRNAs were detected in the retina of OIR mice and 583 miRNAs in the retina of normal control mice. A total of 553 miRNAs were expressed in both groups. Thirty-eight miRNAs showed altered expression in both groups ( p ≤ 0.05 ). Compared with the control group, 2 miRNAs were significantly upregulated in the OIR group, while 36 miRNAs were significantly downregulated. Meanwhile, 2 candidate miRNAs (miR-181a-5p and miR-21a-5p) with significant differences in miRNA expression ( p < 0.01 ) were selected for validation. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to confirm the relative expression of the two miRNAs. Bioinformatics analyses showed that pathways involved in ischemic retinopathy (such as TGF-β, Ras, Hippo, PI3K-Akt, VEGF, and HIF-1 signaling pathways) were enriched. Conclusions. Our study provided an overall view of miRNA profiling in the OIR retina. These miRNA profiles provide a valuable framework for the potential therapy of retinal angiogenesis.
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Haley, Tammie L., Roland Pochet, Larry Baizer, Miriam D. Burton, John W. Crabb, Marc Parmentier, and Arthur S. Polans. "Calbindin D-28K immunoreactivity of human cone cells varies with retinal position." Visual Neuroscience 12, no. 2 (March 1995): 301–7. http://dx.doi.org/10.1017/s0952523800007987.
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AbstractCalbindin D-28K is a calcium-binding protein found in the cone but not rod photoreceptor cells in the retinas of a variety of species. Recent studies of the monkey retina indicated that calbindin D-28K may be expressed preferentially in non-foveal regions of the retina. In the current studies of human retinas, immunohistochemical experiments demonstrated that calbindin D-28K is reduced or absent in the fovea and parafovea, but prevalent in the perifovea and periphery. These findings were supported by the quantification of calbindin D-28K in 1-mm trephine punches obtained from different regions of the human retina. The specificity of the anti-calbindin D-28K antibodies used in these studies was confirmed by Western blot analysis using purified calbindin D-28K. The protein was purified from retinal tissue and its identity confirmed by partial amino-acid sequence analysis. The expression of calbindin D-28K did not correlate with the spectral properties of the cones, rather to their position in the retina. The study of spatially expressed genes, like the one encoding calbindin D-28K, may help explain the patterns of retinal degeneration seen in some human cone-rod dystrophies.
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Gabel-Pfisterer, Amelie. "Operative Therapie der rissbedingten Netzhautablösung – ein Blick in Klinik und Geschichte." Optometry & Contact Lenses 3, no. 7 (August 30, 2023): 246–53. http://dx.doi.org/10.54352/dozv.bkcp8913.
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Purpose. The aim of this clinical article is to describe the surgical treatment of tear-related retinal detachment in the context of the individual retinal findings, the lens status and in consideration of the surgical and postoperative risks, taking into account the specific situation of each patient. Material and Methods. Rhegmatogenous retinal detachment is the result of a retinal tear caused by traction of the vitre- ous on the retina. Liquefied vitreous enters the subretinal space and separates the sensory retina from the pigment epithelium-Bruch’s - membrane complex. As a result, the retina loses contact with the choroid supplying the outer retinal cell layers. The damage caused by the reduced supply, especially to the foveal retina, determines the urgency of surgical treatment. Two very different surgical procedures are available for thera- py: buckling surgery and pars plana vitrectomy. Both surgical methods have different indications and risks and are ex- plained on the basis of our own clinical experience, together with other publications on the same subject, also in their historical context. Results. The treatment goal of rhegmatogenous retinal de- tachment is to bring the retina closer to the retinal pigment epithelium, which ‘pumps out’ the fluid from the subretinal space, and reestablishing the retinas contact to the choroi- dal supply. The entry of fluid into the subretinal space must be permanently prevented by induced scarring. Whether a buckling surgery or a pars plana vitrectomy is indicated depends on the respective retinal findings. The greatest risk after any surgery for a tear-induced retinal detachment is the development of a proliferative vitreoretinopathy and a resulting renewed retinal detachment. Conclusion. Early detection of retinal detachment by the symptoms flashes, floaters, shadows and early binocular oph- thalmoscopy is important to prevent progression of retinal detachment into the fovea and to organize vitreoretinal surgery as soon as possible. The visual prognosis of retinal de- tachments with foveal or macular involvement has improved significantly in the last decades. Keywords Rhegmatogenous retinal detachment, retina surgery, pars plana vitrectomy, denting surgery, retinal break
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Reiter, Chad E. N., Lakshman Sandirasegarane, Ellen B. Wolpert, Marianne Klinger, Ian A. Simpson, Alistair J. Barber, David A. Antonetti, Mark Kester, and Thomas W. Gardner. "Characterization of insulin signaling in rat retina in vivo and ex vivo." American Journal of Physiology-Endocrinology and Metabolism 285, no. 4 (October 2003): E763—E774. http://dx.doi.org/10.1152/ajpendo.00507.2002.
Full textAbstract:
Insulin receptor (IR) signaling cascades have been studied in many tissues, but retinal insulin action has received little attention. Retinal IR signaling and activity were investigated in vivo in rats that were freely fed, fasted, or injected with insulin by phosphotyrosine immunoblotting and by measuring kinase activity. A retina explant system was utilized to investigate the IR signaling cascade, and immunohistochemistry was used to determine which retinal cell layers respond to insulin. Basal IR activity in the retina was equivalent to that in brain and significantly greater than that of liver, and it remained constant between freely fed and fasted rats. Furthermore, IR signaling increased in the retina after portal vein administration of supraphysiological doses of insulin. Ex vivo retinas responded to 10 nM insulin with IR β-subunit (IRβ) and IR substrate-2 (IRS-2) tyrosine phosphorylation and AktSer473 phosphorylation. The retina expresses mRNA for all three Akt isoforms as determined by in situ hybridization, and insulin specifically increases Akt-1 kinase activity. Phospho-AktSer473 immunoreactivity increases in retinal nuclear cell layers with insulin treatment. These results demonstrate that the retinal IR signaling cascade to Akt-1 possesses constitutive activity, and that exogenous insulin further stimulates this prosurvival pathway. These findings may have implications in understanding normal and dysfunctional retinal physiology.
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DU, XIAOHUA, JAMES BLACKAR MAWOLO, and XIA LIU. "Comparison of neuroglobin distribution and expression between the retina of the adult Bactrian camel, rabbits and sheep." Medycyna Weterynaryjna 76, no. 11 (2020): 6473–2020. http://dx.doi.org/10.21521/mw.6473.
Full textAbstract:
Neuroglobin (Ngb) is a kind of protein largely expressed in the brain and retina of mammals. Numerous studies have reported on Ngb expression and distribution in mammals but none have compared the expression in the adult Bactrian camel, rabbits, and sheep. The study examined the distribution and expression of Ngb between the retina of adult Bactrian camel, rabbits, and sheep and provides detailed insight on the morphology of these mammals’ retinae. The immunohistochemical staining procedures were performed to detect Ngb distribution and its expression in the retinae of the adult Bactrian camel, rabbits, and sheep. The results showed that strong positive Ngb expression was found in all layers of the Bactrian camel except the outer nuclear layer, while in the rabbit retina, the strong positive expression was observed in the cortex of the optic nerve fiber layer, the retina cells layer, the network layer, the photoreceptor inner segment, and the pigment, while weak positive expression was shown in the retina of the kernel layer, outside the outer nuclear layer of the retina and the light receptor section. In the adult sheep retina, Ngb was solely expressed in the nerve fiber layer, inner and outer plexiform layer, optic nerve, inner and outer limiting membrane, and photoreceptor inner segment, while weak positive expression was shown in the ganglion cell layer and inner nuclear layer. There exist no Ngb positive expression in the photoreceptor outer segment, the outer nuclear layer, and retinal pigment epithelium of the adult sheep retina. The study documented that Ngb may have a significant function in the maintenance of retinal oxygen homeostasis and participation in the repair of light damage. The study also provided detailed references for Ngb physiological function and its relationship to extreme environmental conditions
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GALLAGHER, SHANNON K., JULIA N. ANGLEN, JUSTIN M. MOWER, and JOZSEF VIGH. "Dopaminergic amacrine cells express opioid receptors in the mouse retina." Visual Neuroscience 29, no. 3 (April 3, 2012): 203–9. http://dx.doi.org/10.1017/s0952523812000156.
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AbstractThe presence of opioid receptors has been confirmed by a variety of techniques in vertebrate retinas including those of mammals; however, in most reports, the location of these receptors has been limited to retinal regions rather than specific cell types. Concurrently, our knowledge of the physiological functions of opioid signaling in the retina is based on only a handful of studies. To date, the best-documented opioid effect is the modulation of retinal dopamine release, which has been shown in a variety of vertebrate species. Nonetheless, it is not known if opioids can affect dopaminergic amacrine cells (DACs) directly, via opioid receptors expressed by DACs. This study, using immunohistochemical methods, sought to determine whether (1) μ- and δ-opioid receptors (MORs and DORs, respectively) are present in the mouse retina, and if present, (2) are they expressed by DACs. We found that MOR and DOR immunolabeling were associated with multiple cell types in the inner retina, suggesting that opioids might influence visual information processing at multiple sites within the mammalian retinal circuitry. Specifically, colabeling studies with the DAC molecular marker anti-tyrosine hydroxylase antibody showed that both MOR and DOR immunolabeling localize to DACs. These findings predict that opioids can affect DACs in the mouse retina directly, via MOR and DOR signaling, and might modulate dopamine release as reported in other mammalian and nonmammalian retinas.
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Kanamoto, Takashi, Yasushi Kitaoka, Hiroaki Sakaue, Yusuke Murakami, Yasuhiro Ikeda, Kei Tobiume, and Yoshiaki Kiuchi. "D-Serine Induced by Ocular Hypertension is Associated with Retinal Cell Death." Current Trends in Ophthalmology 1, no. 1 (July 3, 2018): 23–29. http://dx.doi.org/10.18314/ctoy.v1i1.1161.
Full textAbstract:
Purpose: The purpose of this study is to investigate the role of free D-serine in the death of retinal cells caused by ocular hypertension.Methods: Adult Wistar rats were used as an experimental model of ocular hypertension. Immunohistochemistry was used to identify the retinal sites and expression patterns of D-serine and serine racemase in the rat retina. The concentrations of free D-serine and L-serine in the retina were measured by two-dimensional high-performance liquid chromatography. Retinal cell death was investigated by Immunohistochemistry.Results: D-serine was expressed on the retinal ganglion cell layer in the retinas of rats with ocular hypertension. A serine racemase was specifically expressed in the retinal ganglion cells. The ratio of free D-/L-serine in the retinas with ocular hypertension was higher than that in the retinas with normal tension. Annexing-V-positive cells were observed in the retinal ganglion cell layer in the retinas of the rats with ocular hypertension, and these cells were also co-localized with D-serine expression.Conclusions: We suspect that the up-regulation of serine racemase expression induced by ocular hypertensionleads to an increase in free D-serine converted from free L-serine in retinal ganglion cells and that retinal cell death is associated with D-serine expression.
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Mitchell, C. K., and D. A. Redburn. "Analysis of pre- and postsynaptic factors of the serotonin system in rabbit retina." Journal of Cell Biology 100, no. 1 (January 1, 1985): 64–73. http://dx.doi.org/10.1083/jcb.100.1.64.
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[3H]Serotonin is accumulated by a specific set of amacrine cells in the rabbit retina. These cells also accumulate the neurotoxin, 5,7-dihydroxytryptamine, and show signs of necrosis within 4 h of in vivo exposure to the drug. Biochemical analysis of [3H]serotonin uptake reveal a sodium- and temperature-dependent, high affinity uptake system with a Km of 0.94 microM and Vmax of 1.08 pmol/mg protein/min. [3H]Tryptophan is also accumulated in rabbit retinal homogenates by a high affinity process. Accumulated [3H]serotonin is released in response to potassium-induced depolarization of intact, isolated retinas. In vitro binding studies of rabbit retinal homogenate membranes demonstrate specific sets of binding sites with characteristics of the postsynaptic serotonin receptor. These data strongly suggest that rabbit retina contains virtually all of the molecular components required for a functional serotonergic neurotransmitter system. The only significant difference between the serotonin system in rabbit retina and that in the well-established serotonin transmitter systems in nonmammalin retinas and in brains of most species is the relatively low concentration of endogenous serotonin in rabbit retinas, as demonstrated by high-performance liquid chromatography, histofluorescence, or immunocytochemistry.
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Reinhard, Katja, and Thomas A. Münch. "Visual properties of human retinal ganglion cells." PLOS ONE 16, no. 2 (February 16, 2021): e0246952. http://dx.doi.org/10.1371/journal.pone.0246952.
Full textAbstract:
The retinal output is the sole source of visual information for the brain. Studies in non-primate mammals estimate that this information is carried by several dozens of retinal ganglion cell types, each informing the brain about different aspects of a visual scene. Even though morphological studies of primate retina suggest a similar diversity of ganglion cell types, research has focused on the function of only a few cell types. In human retina, recordings from individual cells are anecdotal or focus on a small subset of identified types. Here, we present the first systematic ex-vivo recording of light responses from 342 ganglion cells in human retinas obtained from donors. We find a great variety in the human retinal output in terms of preferences for positive or negative contrast, spatio-temporal frequency encoding, contrast sensitivity, and speed tuning. Some human ganglion cells showed similar response behavior as known cell types in other primate retinas, while we also recorded light responses that have not been described previously. This first extensive description of the human retinal output should facilitate interpretation of primate data and comparison to other mammalian species, and it lays the basis for the use of ex-vivo human retina for in-vitro analysis of novel treatment approaches.
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Vlasiuk, Anastasiia, and Hiroki Asari. "Feedback from retinal ganglion cells to the inner retina." PLOS ONE 16, no. 7 (July 22, 2021): e0254611. http://dx.doi.org/10.1371/journal.pone.0254611.
Full textAbstract:
Retinal ganglion cells (RGCs) are thought to be strictly postsynaptic within the retina. They carry visual signals from the eye to the brain, but do not make chemical synapses onto other retinal neurons. Nevertheless, they form gap junctions with other RGCs and amacrine cells, providing possibilities for RGC signals to feed back into the inner retina. Here we identified such feedback circuitry in the salamander and mouse retinas. First, using biologically inspired circuit models, we found mutual inhibition among RGCs of the same type. We then experimentally determined that this effect is mediated by gap junctions with amacrine cells. Finally, we found that this negative feedback lowers RGC visual response gain without affecting feature selectivity. The principal neurons of the retina therefore participate in a recurrent circuit much as those in other brain areas, not being a mere collector of retinal signals, but are actively involved in visual computations.
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Mitchell, Cheryl K., and Dianna A. Redburn. "Melatonin inhibits ACh release from rabbit retina." Visual Neuroscience 7, no. 5 (November 1991): 479–86. http://dx.doi.org/10.1017/s0952523800009767.
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AbstractPrevious studies have suggested that melatonin, released from photoreceptors, may modulate retinal dark-adaptive responses by inhibition of dopamine release from retinal interneurons. We have broadened these studies to examine the effect of melatonin on release of another retinal neurotransmitter, acetylcholine (ACh). The ACh system in rabbit retina has been localized to starburst amacrine cells, which release ACh in response to a variety of experimental stimuli, including direct potassium depolarization, flashing light, and glutamatergic as well as GABAergic inputs. The effect of melatonin on release of endogenously synthesized [3H]-ACh was measured in perfusates from retinas or retinal synaptosomes preloaded with [3H]-choline chloride. Melatonin significantly inhibited ACh release stimulated by potassium in intact retina but not in synaptosomes. Stimulation of intact retina by flashing light or by the glutamate receptor agonist, kainic acid, was also inhibited by melatonin. In contrast, there was no significant effect of melatonin on picrotoxin-induced release. These findings suggest that melatonin does have an inhibitory effect on ACh release, either by direct interaction with the cholinergic amacrine cell, or indirectly via GABAergic but not glutamatergic neurons.
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Stier, H., and B. Schlosshauer. "Axonal guidance in the chicken retina." Development 121, no. 5 (May 1, 1995): 1443–54. http://dx.doi.org/10.1242/dev.121.5.1443.
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During retina development, ganglion cells extend their axons exclusively into the innermost tissue layer, but not into outer retina layers. In order to elucidate guiding mechanisms for axons, tissue strips of embryonic chicken retinae were explanted onto retinal cryosections (cryoculture). Ganglion cell axons originating from the explant grew preferentially on the innermost retina layer of cryosections, whereas outer tissue layers were avoided, very much as in vivo. Stereotropism, interaction with laminin of the basal lamina and axonal fasciculation did not significantly affect oriented axonal outgrowth, so that stereotropism as a guidance mechanism could be excluded. Ganglion cell axons were not directed by physical barriers, e.g. microstructured silicon oxide chips. Similarly, UV induced protein inactivation revealed that laminin present in the inner retina did not provide a guidance cue. Even in the absence of ganglion cell axons in retinal cryosections due to prior optic nerve transection in ovo, the growth preference for the innermost retina layer was maintained in cryocultures. However, oriented elongation of axons along the innermost retina layer was lost when radial glial endfeet were selectively eliminated in retinal cryosections. In addition, glial endfeet provided an excellent growth substratum when pure preparations of endfeet were employed in explant cultures. The preference for glial endfeet positioned at the inner retina surface was accompanied by the avoidance of outer retina layers, most likely because of inhibitory components in this region. This assumption is corroborated by the finding that addition of exogenous growth-promoting laminin to cryosections did not abolish the inhibition. Laminin on glass surfaces provided an excellent substratum. Axonal outgrowth was also seriously hampered on specifically purified cells of the outer retina. Most notable, however, in cryocultures aberrant innervation of outer retina layers could be induced by prior heat or protease treatment of cryosections, which pointed to proteins as potential inhibitory components. In summary the data substantiate the hypothesis that within the retina, ganglion cell axons are guided by a dual mechanism based on a permissive and an inhibitory zone. Radial glia is likely to be instructive in this process.
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AlSharari, Shakir, Amal Fatani, Mohammad Ola, Fatima Alrojayee, and Abdulaziz A. Al-Hosaini. "The flavonoid, rutin, ameliorates neurodegeneration in the retina of diabetic rats (CAM1P.164)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 48.21. http://dx.doi.org/10.4049/jimmunol.194.supp.48.21.
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Abstract Diabetic retinopathy remains the leading cause of blindness worldwide. Dietary flavonoid, rutin may protect the diabetes induced retinal damage. The purpose of this study was to examine the ameliorative effect of rutin on diabetic rat retina through neurotrophic, inflammatory and immunological parameters. Diabetes was induced in male Wistar rats by streptozotocin (65mg/kg). Rutin (100mg/kg) was orally administered to normal and diabetic rats after two weeks of diabetes induction and continued for five weeks. After treatments, retinas were isolated and analyzed for potential neuroinflammatory and immunological markers. Our results indicate that the reduced level of brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the diabetic retina were significantly improved by rutin. Increased levels of soluble intracellular adhesion molecule (sICAM-1) and monocyte chemotactic protein (MCP-1) in the diabetic retinas were significantly attenuated to normal level by rutin. Reduced level of GSH in diabetic retina was increased and the increased level of TBARS in the diabetic retina was significantly decreased by rutin administration. The increased level of caspase-3, and decreased level of Bcl-2 in diabetic retina were significantly ameliorated to normal levels by rutin. These results suggest the effectiveness of rutin in protection of diabetic induced damage to the retina by maintaining neurotrophic support, and antioxidants levels.
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CAMERON, DAVID A., and MAUREEN K. POWERS. "Morphology and visual pigment content of photoreceptors from injured goldfish retina." Visual Neuroscience 17, no. 4 (July 2000): 623–30. http://dx.doi.org/10.1017/s0952523800174115.
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Adult teleost fish retinas can regenerate neurons following either surgical or pharmacological injury. The cellular milieu of the damaged retina within which regenerated neurons are produced might be different in these two model systems of retinal injury, and thus the phenotypic attributes of regenerated neurons in the two model systems might also differ. To determine if the phenotypic attributes of photoreceptors, and by extension the recovery of vision, are different between these two model systems, we compared the visual pigment content and morphology of photoreceptors derived from goldfish retinas of both models with control retina. Visual pigments—which consist of a protein moiety (opsin) and a chromophore—were analyzed in single, isolated photoreceptors using microspectrophotometric techniques. We report that visual pigments and photoreceptor morphologies in the surgical model closely matched those of native retina. In contrast, neither photoreceptor morphology nor visual pigment content matched closely in the pharmacological model. The results indicate that phenotypic attributes of photoreceptors can differ significantly between the two model systems of retinal regeneration, but that in both systems, rod- and cone-mediated visual functions can potentially be reestablished.
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Stutzki, Henrike, Florian Helmhold, Max Eickenscheidt, and Günther Zeck. "Subretinal electrical stimulation reveals intact network activity in the blind mouse retina." Journal of Neurophysiology 116, no. 4 (October 1, 2016): 1684–93. http://dx.doi.org/10.1152/jn.01095.2015.
Full textAbstract:
Retinal degeneration ( rd) leads to progressive photoreceptor cell death, resulting in vision loss. Stimulation of the inner-retinal neurons by neuroprosthetic implants is one of the clinically approved vision-restoration strategies, providing basic visual percepts to blind patients. However, little is understood as to what degree the degenerating retinal circuitry and the resulting aberrant hyperactivity may prevent the stimulation of physiological electrical activity. Therefore, we electrically stimulated ex vivo retinas from wild-type ( wt; C57BL/6J) and blind ( rd10 and rd1) mice using an implantable subretinal microchip and simultaneously recorded and analyzed the retinal ganglion cell (RGC) output with a flexible microelectrode array. We found that subretinal anodal stimulation of the rd10 retina and wt retina evoked similar spatiotemporal RGC-spiking patterns. In both retinas, electrically stimulated ON and a small percentage of OFF RGC responses were detected. The spatial selectivity of the retinal network to electrical stimuli reveals an intact underlying network with a median receptive-field center of 350 μm in both retinas. An antagonistic surround is activated by stimulation with large electrode fields. However, in rd10 and to a higher percentage, in rd1 retinas, rhythmic and spatially unconfined RGC patterns were evoked by anodal or by cathodal electrical stimuli. Our findings demonstrate that the surviving retinal circuitry in photoreceptor-degenerated retinas is preserved in a way allowing for the stimulation of temporally diverse and spatially confined RGC activity. Future vision restoration strategies can build on these results but need to avoid evoking the easily inducible rhythmic activity in some retinal circuits.
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Antonio, Erivaldo A., Fabrício B. de Sá, Katharine R. P. Santos, Nivaldo B. Lima Junior, Fabricya R. Silva, Francisco C. A. Aguiar Júnior, and Jeymesson R. C. Vieira. "Comparative retinal histomorphometry and visual acuity of three bat species of the genus Artibeus (Phyllostomidae: Stenodermatinae)." Pesquisa Veterinária Brasileira 40, no. 11 (November 2020): 933–45. http://dx.doi.org/10.1590/1678-5150-pvb-6701.
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ABSTRACT: This study performed a histomorphometric analysis of the retina and estimated the visual acuity of three fruit-eating bats of the genus Artibeus, including Artibeus lituratus, Artibeus planirostris and Artibeus obscurus. In total, 13 animals were used for this study, in which the retinas were hemidisected, fixed, cut, and stained. The visual acuity was determined by the density of ganglion cells in the retina and the retinal layers were also measured from histological sections. The retinas of these bats are avascular, do not present tapetum lucidum in any quadrant, and have the 10 retinal layers common in mammals. Moreover, it was observed that the thickness of the retina in the central region was significantly higher in all measured parameters (p<0.001), except for the outer plexiform layer (OPL) which was significantly higher in the peripheral region (p<0.001). The retinas of the three species showed a horizontal visual streak with a higher concentration of retinal ganglion cells (RGCs) at the inferotemporal region. In addition, the species A. lituratus exhibited extras areas of high cell density in the retina. Thus, A. lituratus showed the highest visual acuity (1.92 cycles/degree), while A. planirostris showed a visual acuity of (1.77 cycles/degree) and A. obscurus exhibited the lowest visual acuity (1.50 cycles/degree). All these characteristics are related to the echolocation system and the eating habits of each species. Therefore, it can be concluded that bats of the genus Artibeus have a high visual acuity value compared to other echolocating bats and all these differences might be directly linked to the phylogeny of the genus.
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Feng, Yuxi, Shalini Gross, Anupriya Chatterjee, Yumei Wang, Jihong Lin, and Hans-Peter Hammes. "Transcription of Inflammatory Cytokine TNFα is Upregulated in Retinal Angiogenesis under Hyperoxia." Cellular Physiology and Biochemistry 39, no. 2 (2016): 573–83. http://dx.doi.org/10.1159/000445649.
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Background/Aims: Hypoxia induces angiogenesis while hyperoxia promotes vasoregression in the retina. We investigated herein the effect of prolonged hyperoxia on retinal angiogenesis and the underlying mechanism in an oxygen-induced retinopathy (OIR) model. Methods: Vascular morphology was quantified in whole-mount retina from the mice subjected to the conventional OIR model (c-OIR) or the OIR model with prolonged hyperoxia (p-OIR). Expressions of genes related to angiogenesis were determined by real-time PCR. Results: p-OIR retinas showed few intraretinal neovascular tufts at the border of avascular zones, lacking preretinal neovascularization, whereas c-OIR retinas had numerous preretinal neovascularizations. p-OIR retinas demonstrated outgrowth of capillaries in the deep layers despite persistent hyperoxia and possess a larger avascular zone compared with the c-OIR retinas. The capillaries in the p-OIR retinas were well-formed in contrast to those in the c-OIR retinas. p-OIR retinas expressed significantly higher TNFα (∼4 fold) than c-OIR retinas. The expression of vascular endothelial growth factor, Erythropoietin, Angiopoietin 1 and 2 remained unchanged. Conclusion: Our data demonstrate that TNFα transcription is increased in hyperoxia-promoted retinal angiogenesis, implicating it, in association with low VEGF levels, as a possible proponent in retinal angiogenesis under hyperoxia.
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Wagner, Natalie, Armin Safaei, Pia A. Vogt, Maurice R. Gammel, H. Burkhard Dick, Sven Schnichels, and Stephanie C. Joachim. "Coculture of ARPE-19 Cells and Porcine Neural Retina as an Ex Vivo Retinal Model." Alternatives to Laboratory Animals 50, no. 1 (January 2022): 27–44. http://dx.doi.org/10.1177/02611929221082662.
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Neural retinal organ cultures are used to investigate ocular pathomechanisms. However, these cultures lack the essential retinal pigment epithelium (RPE) cells, which are part of the actual in vivo retina. To simulate a more realistic ex vivo model, porcine neural retina explants were cocultured with ARPE-19 cells (ARPE-19 group), which are derived from human RPE. To identify whether the entire cells or just the cell factors are necessary, in a second experimental group, porcine neural retina explants were cultured with medium derived from ARPE-19 cells (medium group). Individually cultured neural retina explants served as controls (control group). After 8 days, all neural retinas were analysed to evaluate retinal thickness, photoreceptors, microglia, complement factors and synapses ( n = 6–8 per group). The neural retina thickness in the ARPE-19 group was significantly better preserved than in the control group ( p = 0.031). Also, the number of L-cones was higher in the ARPE-19 group, as compared to the control group ( p < 0.001). Furthermore, the ARPE-19 group displayed an increased presynaptic glutamate uptake (determined via vGluT1 labelling) and enhanced post-synaptic density (determined via PSD-95 labelling). Combined Iba1 and iNOS detection revealed only minor effects of ARPE-19 cells on microglial activity, with a slight downregulation of total microglia activity apparent in the medium group. Likewise, only minor beneficial effects on photoreceptors and synaptic structure were found in the medium group. This novel system offers the opportunity to investigate interactions between the neural retina and RPE cells, and suggests that the inclusion of a RPE feeder layer has beneficial effects on the ex vivo maintenance of neural retina. By modifying the culture conditions, this coculture model allows a better understanding of photoreceptor death and photoreceptor–RPE cell interactions in retinal diseases.
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Sitaramayya, Ari, Lorraine Lombardi, and Alexander Margulis. "Influence of dopamine on cyclic nucleotide enzymes in bovine retinal membrane fractions." Visual Neuroscience 10, no. 6 (November 1993): 991–96. http://dx.doi.org/10.1017/s0952523800010099.
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AbstractDopamine is a major neurotransmitter and neuromodulator in vertebrate retina. Although its pharmacological and physiological actions are well understood, the biochemical mechanisms of its signal transduction are less clear. Acting via D1 receptors, dopamine was shown to increase cyclic AMP levels in intact retina and to activate adenylate cyclase in retinal homogenates. The action via activation of D2 receptors is controversial: it was reported to decrease cyclic AMP levels in intact retina but inhibition of cyclase could not be demonstrated in retinal homogenates; also it was reported to activate rod outer segment cyclic GMP phosphodiesterase in vitro but did not decrease cyclic GMP levels in aspartate-treated retinas. We made an attempt to fractionate bovine retinal membranes and to investigate the effects of dopamine, via Dl and D2 receptors, on the synthesis and hydrolysis of cyclic AMP and cyclic GMP. Activation of cyclic AMP synthesis was noted in all fractions, but no effects were evident on cyclic nucleotide hydrolysis or cyclic GMP synthesis in any fraction. Also, D2 agonist did not inhibit cyclic AMP synthesis. These observations suggest that D2 receptors may not be directly coupled to cyclic nucleotide metabolizing enzymes in bovine retina.
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Yan, Qi, E. Helene Sage, and Anita E. Hendrickson. "SPARC Is Expressed by Ganglion Cells and Astrocytes in Bovine Retina." Journal of Histochemistry & Cytochemistry 46, no. 1 (January 1998): 3–10. http://dx.doi.org/10.1177/002215549804600102.
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SPARC (secreted protein, acidic and rich in cysteine)/osteonectin is a matricellular, counteradhesive glycoprotein that disrupts cell-matrix interactions, interacts with growth factors and components of extracellular matrix, and modulates the cell cycle, but appears to subserve only minor structural roles. SPARC is expressed in a variety of tissues during embryogenesis and remodeling and is believed to regulate vascular morphogenesis and cellular differentiation. Although usually limited in normal adult tissues, SPARC is expressed at significant levels in the adult central nervous system. Using a monoclonal antibody against bovine bone osteonectin, we have determined the localization of SPARC in newborn (3-day-old) and adult (4–8-year-old) normal bovine retinas. SPARC was present in the soma of ganglion cells and strong reactivity was found in ganglion cell axons. Muller cells displayed no immunoreactivity, but SPARC was present in retinal astrocytes that were identified by the astrocyte marker glial fibrillary acidic protein (GFAP). Newborn calf retina showed a staining pattern similar to that of adult retina but exhibited significantly reduced levels of SPARC. Minimal levels of SPARC protein were also detected in some capillaries of the inner retina of both newborn and adult animals, whereas large vessels were negative. The presence of SPARC in the retina was confirmed by Western blotting of retinal extracts. These data indicate that SPARC originating from both neurons and glia of the inner retina may be an important modulator of retinal angiogenesis. The increased expression of SPARC in adult relative to newborn retinal tissue also indicates that SPARC has an ongoing role in the maintainance of retinal functions.
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Alrifaee, Zainab Ibrahim Abood, and Tarik Zeyad Ismaeel. "Cryptography based on retina information." Indonesian Journal of Electrical Engineering and Computer Science 28, no. 3 (October 7, 2022): 1697. http://dx.doi.org/10.11591/ijeecs.v28.i3.pp1697-1708.
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The security of message information has drawn more attention nowadays, so; cryptography has been used extensively. This research aims to generate secured cipher keys from retina information to increase the level of security. The proposed technique utilizes cryptography based on retina information. The main contribution is the original procedure used to generate three types of keys in one system from the retina vessel's end position and improve the technique of three systems, each with one key. The distances between the center of the diagonals of the retina image and the retina vessel's end (diagonal center-end (DCE)) represent the first key. The distances between the center of the radius of the retina and the retina vessel's end (radius center-end (RCE)) represent the second key. While the diagonal-radius center and the retina vessel's end (diagonal-radius center-end (DRCE)) represent the third key. The results illustrate the process's validity and applicability. Also, improve the time required to decrypt the cipher-text by a brute force attack (BFA) from (4.358e+139) year in the compared technique to (1.3074e+140) year for retina3. The BFA time will increase with increasing the number of retina vessels, as in retina1, 2, and 3, which have 24, 53, and 103 retina vessels.
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KRYGER, Z., L. GALLI-RESTA, G. H. JACOBS, and B. E. REESE. "The topography of rod and cone photoreceptors in the retina of the ground squirrel." Visual Neuroscience 15, no. 4 (April 1998): 685–91. http://dx.doi.org/10.1017/s0952523898154081.
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The distributions of rod and cone photoreceptors have been determined in the retina of the California ground squirrel, Spermophilus beecheyi. Retinas were fixed by perfusion and the rods and cones were detected with indirect immunofluorescence using opsin antibodies. Local densities were determined at 2-mm intervals across the entire retina, from which total numbers of each receptor type were estimated and isodensity distributions were constructed. The ground squirrel retina contains 7.5 million cones and 1.27 million rods. The peak density for the cones (49,550/mm2) is found in a horizontal strip of central retina 2 mm ventral to the elongated optic nerve head, falling gradually to half this value in the dorsal and ventral retinal periphery. Of the cones, there are 14 M cones for every S cone. S cone density is relatively flat across most of the retina, reaching a peak (4500/mm2) at the temporal end of the visual streak. There is one exception to this, however: S cone density climbs dramatically at the extreme dorso-nasal retinal margin (20,000/mm2), where the local ratio of S to M cones equals 1. Rod density is lowest in the visual streak, where the rods comprise less than 5% of the local photoreceptor population, increasing conspicuously in the ventral retina, where the rods achieve 30% of the local photoreceptor population (13,000/mm2). The functional importance of the change in S to M cone ratio at the dorsal circumference of the retina is compromised by the extremely limited portion of the visual field subserved by this retinal region. The significance for vision, if any, remains to be determined. By contrast, the change in rod/cone ratio between the dorsal and ventral halves of the retina indicates a conspicuous asymmetry in the ground squirrel's visual system, suggesting a specialization for maximizing visual sensitivity under dim levels of illumination in the superior visual field.
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Weitz, Andrew C., Matthew R. Behrend, Nan Sook Lee, Ronald L. Klein, Vince A. Chiodo, William W. Hauswirth, Mark S. Humayun, James D. Weiland, and Robert H. Chow. "Imaging the response of the retina to electrical stimulation with genetically encoded calcium indicators." Journal of Neurophysiology 109, no. 7 (April 1, 2013): 1979–88. http://dx.doi.org/10.1152/jn.00852.2012.
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Epiretinal implants for the blind are designed to stimulate surviving retinal neurons, thus bypassing the diseased photoreceptor layer. Single-unit or multielectrode recordings from isolated animal retina are commonly used to inform the design of these implants. However, such electrical recordings provide limited information about the spatial patterns of retinal activation. Calcium imaging overcomes this limitation, as imaging enables high spatial resolution mapping of retinal ganglion cell (RGC) activity as well as simultaneous recording from hundreds of RGCs. Prior experiments in amphibian retina have demonstrated proof of principle, yet experiments in mammalian retina have been hindered by the inability to load calcium indicators into mature mammalian RGCs. Here, we report a method for labeling the majority of ganglion cells in adult rat retina with genetically encoded calcium indicators, specifically GCaMP3 and GCaMP5G. Intravitreal injection of an adeno-associated viral vector targets ∼85% of ganglion cells with high specificity. Because of the large fluorescence signals provided by the GCaMP sensors, we can now for the first time visualize the response of the retina to electrical stimulation in real-time. Imaging transduced retinas mounted on multielectrode arrays reveals how stimulus pulse shape can dramatically affect the spatial extent of RGC activation, which has clear implications in prosthetic applications. Our method can be easily adapted to work with other fluorescent indicator proteins in both wild-type and transgenic mammals.
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Sinha, Tirthankar, Jianhai Du, Mustafa S. Makia, James B. Hurley, Muna I. Naash, and Muayyad R. Al-Ubaidi. "Absence of retbindin blocks glycolytic flux, disrupts metabolic homeostasis, and leads to photoreceptor degeneration." Proceedings of the National Academy of Sciences 118, no. 6 (February 1, 2021): e2018956118. http://dx.doi.org/10.1073/pnas.2018956118.
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We previously reported a model of progressive retinal degeneration resulting from the knockout of the retina-specific riboflavin binding protein, retbindin (Rtbdn−/−). We also demonstrated a reduction in neural retinal flavins as a result of the elimination of RTBDN. Given the role of flavins in metabolism, herein we investigated the underlying mechanism of this retinal degeneration by performing metabolomic analyses on predegeneration at postnatal day (P) 45 and at the onset of functional degeneration in the P120 retinas. Metabolomics of hydrophilic metabolites revealed that individual glycolytic products accumulated in the P45 Rtbdn−/− neural retinas along with the elevation of pentose phosphate pathway, while TCA cycle intermediates remained unchanged. This was confirmed by using 13C-labeled flux measurements and immunoblotting, revealing that the key regulatory step of phosphoenolpyruvate to pyruvate was inhibited via down-regulation of the tetrameric pyruvate kinase M2 (PKM2). Separate metabolite assessments revealed that almost all intermediates of acylcarnitine fatty acid oxidation, ceramides, sphingomyelins, and multiple toxic metabolites were significantly elevated in the predegeneration Rtbdn−/− neural retina. Our data show that lack of RTBDN, and hence reduction in flavins, forced the neural retina into repurposing glucose for free-radical mitigation over ATP production. However, such sustained metabolic reprogramming resulted in an eventual metabolic collapse leading to neurodegeneration.
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Lillien, L., and C. Cepko. "Control of proliferation in the retina: temporal changes in responsiveness to FGF and TGF alpha." Development 115, no. 1 (May 1, 1992): 253–66. http://dx.doi.org/10.1242/dev.115.1.253.
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Proliferation in the rat retina, as in other parts of the nervous system, occurs during a restricted period of development. In addition to regulating cell number, the mechanisms that control proliferation influence the patterning of tissues, and may affect the determination of cell type. To begin to determine how proliferation is controlled, several growth factors found in the retina were tested for effects on progenitor cell division in culture. Proliferation was enhanced by TGF alpha, bFGF and aFGF, and many of the dividing cells later differentiated into cells with the antigenic phenotypes of retinal neurons and glial cells. The mitotic response of retinal cells to these factors changed during development: progenitor cells from younger retinas (embryonic day 15 to 18; E15-E18) were more responsive to FGF's, while progenitor cells from older retinas (greater than E20) were more responsive to TGF alpha. Progenitor cells stopped dividing in vitro, even when treated with excess mitogen. These observations suggest that proliferation in the retina may be stimulated by multiple mitogenic signals provided by TGF alpha, FGF, or related factors, and that proliferation is not controlled by limiting concentrations of mitogen alone. Rather, these data demonstrate that retinal cells change during development in their responsiveness to mitogenic signals. Such changes may contribute to the regulation of proliferation.
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Hurley, James B. "Retina Metabolism and Metabolism in the Pigmented Epithelium: A Busy Intersection." Annual Review of Vision Science 7, no. 1 (September 15, 2021): 665–92. http://dx.doi.org/10.1146/annurev-vision-100419-115156.
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The outer retina is nourished from the choroid, a capillary bed just inside the sclera. O2, glucose, and other nutrients diffuse out of the choroid and then filter through a monolayer of retinal pigment epithelium (RPE) cells to fuel the retina. Recent studies of energy metabolism have revealed striking differences between retinas and RPE cells in the ways that they extract energy from fuels. The purpose of this review is to suggest and evaluate the hypothesis that the retina and RPE have complementary metabolic roles that make them depend on each other for survival and for their abilities to perform essential and specialized functions.
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Tatsumi, Tomoaki, Takayuki Baba, Hirotaka Yokouchi, and Shuichi Yamamoto. "Nonperfused Peripheral Retinal Area in Eyes with Chronic Rhegmatogenous Retinal Detachment." Case Reports in Ophthalmology 11, no. 2 (July 28, 2020): 385–90. http://dx.doi.org/10.1159/000509157.
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We report two cases of chronic rhegmatogenous retinal detachment with a nonperfused peripheral retinal area. Case 1 was an 84-year-old woman who presented with a bullous retinal detachment of the inferior retina and a best-corrected visual acuity of 20/500. A small horseshoe tear was detected in the peripheral superior retina. Fluorescein angiography showed a wide area of nonperfused retina in the inferior retina. The retina was successfully reattached by scleral buckling surgery. Case 2 was a 40-year-old woman who presented with a shallow retinal detachment involving the macula. There were multiple retinal breaks at the pars plana that were secondary to blunt trauma. Fluorescein angiography revealed a wide area of nonperfused retina in the inferior peripheral retina. She underwent scleral buckling surgery, and the retina was successfully reattached. Our findings indicate that clinicians should examine the peripheral retina carefully especially with fluorescein angiography to search for nonperfused areas in eyes with chronic rhegmatogenous retinal detachment.