Journal articles on the topic 'Inner retina'
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1
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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Acosta, Monica L., Michael Kalloniatis, and David L. Christie. "Creatine transporter localization in developing and adult retina: importance of creatine to retinal function." American Journal of Physiology-Cell Physiology 289, no. 4 (October 2005): C1015—C1023. http://dx.doi.org/10.1152/ajpcell.00137.2005.
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Creatine and phosphocreatine are required to maintain ATP needed for normal retinal function and development. The aim of the present study was to determine the distribution of the creatine transporter (CRT) to gain insight to how creatine is transported into the retina. An affinity-purified antibody raised against the CRT was applied to adult vertebrate retinas and to mouse retina during development. Confocal microscopy was used to identify the localization pattern as well as co-localization patterns with a range of retinal neurochemical markers. Strong labeling of the CRT was seen in the photoreceptor inner segments in all species studied and labeling of a variety of inner neuronal cells (amacrine, bipolar, and ganglion cells), the retinal nerve fibers and sites of creatine transport into the retina (retinal pigment epithelium, inner retinal blood vessels, and perivascular astrocytes). The CRT was not expressed in Müller cells of any of the species studied. The lack of labeling of Müller cells suggests that neurons are independent of this glial cell in accumulating creatine. During mouse retinal development, expression of the CRT progressively increased throughout the retina until approximately postnatal day 10, with a subsequent decrease. Comparison of the distribution patterns of the CRT in vascular and avascular vertebrate retinas and studies of the mouse retina during development indicate that creatine and phosphocreatine are important for ATP homeostasis.
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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.
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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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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.
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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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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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Yu, Dao-Yi, and Stephen J. Cringle. "Low oxygen consumption in the inner retina of the visual streak of the rabbit." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H419—H423. http://dx.doi.org/10.1152/ajpheart.00643.2003.
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The oxygen requirements of different retinal layers are of interest in understanding the vulnerability of the retina to hypoxic damage in retinal diseases with an ischemic component. Here, we report the first measurements of retinal oxygen consumption in the visual streak of the rabbit retina, the region with the highest density of retinal neurons, and compare it with that in the less-specialized region of the retina underlying the vascularized portion of the rabbit retina. Oxygen-sensitive microelectrodes were used to measure oxygen tension as a function of retinal depth in anesthetized animals. Measurements were performed in the region of the retina containing overlying retinal vessels and in the center of the visual streak. Established mathematical analyses of the intraretinal oxygen distribution were used to quantify the rate of oxygen consumption in the inner and outer retina and the relative oxygen contributions from the choroidal and vitreal sides. Outer retinal oxygen consumption was higher in the visual streak than in the vascularized area (means ± SE, 284 ± 20 vs. 210 ± 23 nl O2·min–1·cm–2, P = 0.026, n = 10). However, inner retinal oxygen consumption in the visual streak was significantly lower than in the vascular area (57 ± 4.3 vs. 146 ± 12 nl O2·min–1·cm–2, P < 0.001). We conclude that despite the higher processing requirements of the inner retina in the visual streak, it has a significantly lower oxygen consumption rate than the inner retina underlying the retinal vasculature. This suggests that the oxygen uptake of the inner retina is regulated to a large degree by the available oxygen supply rather than the processing requirements of the inner retina alone.
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SPRINGER, A. D., and A. E. HENDRICKSON. "Development of the primate area of high acuity. 2. Quantitative morphological changes associated with retinal and pars plana growth." Visual Neuroscience 21, no. 5 (September 2004): 775–90. http://dx.doi.org/10.1017/s0952523804215115.
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Mechanisms underlying the development of the primate area of high acuity (AHA) remain poorly understood. Finite-element models have identified retinal stretch and intraocular pressure (IOP) as possible mechanical forces that can form a pit (Springer & Hendrickson, 2004). A series ofMacaca nemestrinamonkey retinas between 68 days postconception (dpc) and adult were used to quantify growth and morphological changes. Retinal and pars plana length, optic disc diameter, disc-pit distance, and inner and outer retinal laminar thickness were measured over development to identify when and where IOP or stretch might operate. Horizontal optic disc diameter increased 500 μm between 115 dpc and 2 months after birth when it reached adult diameter. Disc growth mainly influences the immediate surrounding retina, presumably displacing retinal tissue centrifugally. Pars plana elongation also began at 115 dpc and continued steadily to 3–4 years postnatal, so its influence would be relatively constant over retinal development. Unexpectedly, horizontal retinal length showed nonlinear growth, divided into distinct phases. Retinal length increased rapidly until 115 dpc and then remained unchanged (quiescent phase) between 115–180 dpc. After birth, the retina grew rapidly for 3 months and then very slowly into adulthood. The onset of pit development overlapped the late fetal quiescent phase, suggesting that the major mechanical factor initiating pit formation is IOP, not retinal growth-induced stretch. Developmental changes in the thickness of retinal layers were different for inner and outer retina at many, but not all, of the ten eccentricities examined. Peripheral inner and outer retinal layers thinned appreciably with age, consistent with retinal stretch having a larger effect on the retinal periphery. Central inner retina around the area of high acuity (AHA) changed tri-phasically. It increased in thickness prenatally, thinned transiently after birth, and then resumed thickening. Transient postnatal inner retinal thinning around the pit coincided with the resumption of retinal growth and with cone packing providing evidence that a small amount of growth-induced central retinal stretch may account for cone packing as previously hypothesized (Springer, 1999). Central outer retina around the AHA progressively thickened over the fetal period. It reached asymptotic thickness at birth and continued to thicken into adulthood at some temporal, but not nasal, central eccentricities. These data indicate that peripheral outer and inner retina progressively thin with age because of eye growth-induced stretch, while central retina is minimally affected by stretch. Outer and inner retinal laminar thickness at the same locus can change in different directions, suggesting that they shear with respect to one another. This shearing induces the elongation of Henle axons, while their angle reflects the direction of shear.
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Saari, John C., Robert J. Champer, Mary Ann Asson-Batres, Gregory G. Garwin, Jing Huang, John W. Crabb, and Ann H. Milam. "Characterization and localization of an aldehyde dehydrogenase to amacrine cells of bovine retina." Visual Neuroscience 12, no. 2 (March 1995): 263–72. http://dx.doi.org/10.1017/s095252380000794x.
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AbstractAn enzyme of bovine retina that catalyzes oxidation of retinaldehyde to retinoic acid was purified to homogeneity and a monoclonal antibody (mAb H-4) was generated. MAb H-4 recognized a single component (Mr = 55,000) in extracts of bovine retina and other bovine tissues. The antibody showed no cross-reactivity with extracts of rat, monkey, or human retinas. A 2067 bp cDNA was selected from a retina cDNA expression library using mAb H-4. The cDNA hybridized with a similarly sized, moderately abundant mRNA prepared from bovine retina. Nucleotide sequence analysis indicated that the cDNA contained a single open reading frame encoding 501 amino acids that have 88% sequence identity with the amino-acid sequence of human hepatic Class 1 aldehyde dehydrogenase. Amino-acid sequence analysis of purified enzyme demonstrated that the cDNA encodes the isolated enzyme. MAb H-4 specifically labeled the somata and processes of a subset of amacrine cells in bovine retinal sections. Labeled amacrine somata were located on both sides of the inner plexiform layer, and their processes ramified into two laminae within the inner plexiform layer. The inner radial processes of Müller (glial) cells were weakly reactive with mAb H-4. Weak immunostaining of amacrine cells was found in monkey retina with mAb H-4, but no signal was detected in rat or human retina. The results provide further evidence for metabolism and function of retinoids within cells of the inner retina and define a novel class of retinal amacrine cells.
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BARNARD, ALUN R., JOANNE M. APPLEFORD, SUMATHI SEKARAN, KRISHNA CHINTHAPALLI, AARON JENKINS, MATHEAS SEELIGER, MARTIN BIEL, et al. "Residual photosensitivity in mice lacking both rod opsin and cone photoreceptor cyclic nucleotide gated channel 3 α subunit." Visual Neuroscience 21, no. 5 (September 2004): 675–83. http://dx.doi.org/10.1017/s0952523804215024.
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The mammalian retina contains three classes of photoreceptor. In addition to the rods and cones, a subset of retinal ganglion cells that express the putative sensory photopigment melanopsin are intrinsically photosensitive. Functional and anatomical studies suggest that these inner retinal photoreceptors provide light information for a number of non-image-forming light responses including photoentrainment of the circadian clock and the pupil light reflex. Here, we employ a newly developed mouse model bearing lesions of both rod and cone phototransduction cascades (Rho−/−Cnga3−/−) to further examine the function of these non-rod non-cone photoreceptors. Calcium imaging confirms the presence of inner retinal photoreceptors inRho−/−Cnga3−/−mice. Moreover, these animals retain a pupil light reflex, photoentrainment, and light induction of the immediate early genec-fosin the suprachiasmatic nuclei, consistent with previous findings that pupillary and circadian responses can employ inner retinal photoreceptors.Rho−/−Cnga3−/−mice also show a light-dependent increase in the number of FOS-positive cells in both the ganglion cell and (particularly) inner nuclear layers of the retina. The average number of cells affected is several times greater than the number of melanopsin-positive cells in the mouse retina, suggesting functional intercellular connections from these inner retinal photoreceptors within the retina. Finally, however, while we show that wild types exhibit an increase in heart rate upon light exposure, this response is absent inRho−/−Cnga3−/−mice. Thus, it seems that non-rod non-cone photoreceptors can drive many, but not all, non-image-forming light responses.
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Cahill, Gregory M., and Joseph C. Besharse. "Light-sensitive melatonin synthesis by Xenopus photoreceptors after destruction of the inner retina." Visual Neuroscience 8, no. 5 (May 1992): 487–90. http://dx.doi.org/10.1017/s0952523800005009.
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AbstractSeveral lines of evidence indicate that retinal photoreceptors produce melatonin. However, there are other potential melatonin sources in the retina, and melatonin synthesis can be regulated by feedback from the inner retina. To analyze cellular mechanisms of melatonin regulation in retinal photoreceptors, we have developed an in vitro method for destruction of the inner retina that preserves functional photoreceptors in contact with the pigment epithelium. Eyecups, which include the neural retina, retinal pigment epithelium, choroid, and sclera were prepared. The vitreal surface of the retina in each eyecup was washed sequentially with 1% Triton X-100, water, and culture medium. This lysed the ganglion cells and neurons and glia of the inner nuclear layer, causing the retina to split apart within the inner nuclear layer. The damaged inner retina was peeled away, leaving photoreceptors attached to the pigment epithelium. The cell density of the inner nuclear layer was reduced 94% by this method, but there was little apparent damage to the photoreceptors. Lesioned eyecups produced normal melatonin levels in darkness at night, and melatonin production was inhibited by light. These results indicate that the inner retina is not necessary for melatonin production nor for regulation of photoreceptor melatonin synthesis by light. The lesion method used in this study may be useful for other physiological and biochemical studies of photoreceptors.
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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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Karwoski, C. J., D. A. Frambach, and L. M. Proenza. "Laminar profile of resistivity in frog retina." Journal of Neurophysiology 54, no. 6 (December 1, 1985): 1607–19. http://dx.doi.org/10.1152/jn.1985.54.6.1607.
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Measurements of absolute transretinal resistance and of the relative resistance of the various retinal layers were obtained in the frog. The resistance of clamped sections of isolated retina was 66 omega . cm2, which results in an average resistivity (rho) between inner and outer limiting membranes of 5,050 omega . cm. In eyecups, relative resistances (obtained by passing constant currents across the retina) were assigned to specific layers of the retina with the aid of physiological criteria (e.g., depths of light-evoked field potentials, changes in extracellular K+ concentration, base-line noise level, and resistance). These relative resistances were then converted to absolute values, a calculation feasible because the region between inner and outer limiting membranes, which has the same structure in both isolated and eyecup retinas, could be specified during experiments. Resistivities (in omega . cm) for the retinal layers include 1) subretinal space, 970; 2) inner and outer nuclear layers, 6,800; and 3) inner plexiform layer, 1,750. The ganglion cell and optic nerve fiber layers were too thin to resolve individually, but rho of the two layers combined was 7,900. The outer plexiform layer was also too thin to reliably resolve, but its rho is likely the same as the inner plexiform layer. The extracellular space volume fraction (alpha) of the retinal layers was estimated from these rho s, and the following values were obtained: 1) subretinal space, 0.12; 2) outer and inner nuclear layers, 0.03; 3) inner and outer plexiform layers, 0.11; and 4) ganglion cell and optic nerve fiber layers, 0.02. The decreased rho and increased alpha of the inner plexiform layer and the subretinal space, compared with that of the nuclear layers, are expected from their anatomy. A consideration of these inhomogeneities is required in analyses of field potentials and of changes in extracellular ionic concentrations.
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MacNEIL, MARGARET A., SHERYL PURRIER, and R. JARRETT RUSHMORE. "The composition of the inner nuclear layer of the cat retina." Visual Neuroscience 26, no. 4 (July 2009): 365–74. http://dx.doi.org/10.1017/s0952523809990162.
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AbstractThe cellular composition of the inner nuclear layer (INL) is largely conserved among mammals. Studies of rabbit, monkey, and mouse retinas have shown that bipolar, amacrine, Müller, and horizontal cells make up constant fractions of the INL (42, 35, 20, and 3%, respectively); these proportions remain relatively constant at all retinal eccentricities. The purpose of our study was to test whether the organization of cat retina is similar to that of other mammalian retinas. Fixed retinas were embedded in plastic, serially sectioned at a thickness of 1 μm, stained, and imaged at high power in the light microscope. Bipolar, amacrine, Müller, and horizontal cells were classified and counted according to established morphological criteria. Additional sets of sections were processed for protein kinase C and calretinin immunoreactivity to determine the relative fraction of rod bipolar and AII amacrine cells. Our results show that the organization of INL in the cat retina contains species-specific alterations in the composition of the INL tied to the large fraction of rod photoreceptors. Compared with other mammalian retinas, cat retinas show an expansion of the rod pathway with rod bipolar cells accounting for about 70% of all bipolar cells and AII cells accounting for nearly a quarter of all amacrine cells. Our results suggest that evolutionary pressures in cats over time have refined their retinal organization to suit its ecological niche.
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LI, BAOQIN, KELLI McKERNAN, and WEN SHEN. "Spatial and temporal distribution patterns of Na-K-2Cl cotransporter in adult and developing mouse retinas." Visual Neuroscience 25, no. 2 (March 2008): 109–23. http://dx.doi.org/10.1017/s0952523808080164.
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AbstractThe Na-K-2Cl cotransporter (NKCC) is a Cl− uptake transporter that is responsible for maintaining a Cl− equilibrium potential positive to the resting potential in neurons. If NKCC is active, GABA and glycine can depolarize neurons. In view of the abundance of GABAergic and glycinergic synapses in retina, we undertook a series of studies using immunocytochemical techniques to determine the distribution of NKCC in retinas of both developing and adult mice. We found NKCC antibody (T4) labeling present in retinas from wild-type mice, but not in NKCC1-deficient mice, suggesting that the NKCC1 subtype is a major Cl− uptake transporter in mouse retina. Strong labeling of NKCC1 was present in horizontal cells and rod-bipolar dendrites in adult mice. Interestingly, we also found that a diffuse labeling pattern was present in photoreceptor terminals. However, NKCC1 was barely detectable in the inner retina of adult mice. Using an antibody against K-Cl cotransporter 2 (KCC2), we found that KCC2, a transporter that extrudes Cl−, was primarily expressed in the inner retina. The expression of NKCC1 in developing mouse retinas was studied from postnatal day (P) 1 to P21, NKCC1 labeling first appeared in the dendrites of horizontal and rod-bipolar cells as early as P7, followed by photoreceptor terminals between P10-P14; with expression gradually increasing concomitantly with the growth of synaptic terminals and dendrites throughout retinal development. In the inner retina, NKCC1 labeling was initially observed in the inner plexiform layer at P1, but labeling diminished after P5. The developmental increase in NKCC expression only occurred in the outer retina. Our results suggest that the distal synapses and synaptogenesis in mouse retinas undergo a unique process with a high intracellular Cl− presence due to NKCC1 expression.
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Yemanyi, Felix, Kiran Bora, Alexandra K. Blomfield, Zhongxiao Wang, and Jing Chen. "Wnt Signaling in Inner Blood–Retinal Barrier Maintenance." International Journal of Molecular Sciences 22, no. 21 (November 2, 2021): 11877. http://dx.doi.org/10.3390/ijms222111877.
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The retina is a light-sensing ocular tissue that sends information to the brain to enable vision. The blood–retinal barrier (BRB) contributes to maintaining homeostasis in the retinal microenvironment by selectively regulating flux of molecules between systemic circulation and the retina. Maintaining such physiological balance is fundamental to visual function by facilitating the delivery of nutrients and oxygen and for protection from blood-borne toxins. The inner BRB (iBRB), composed mostly of inner retinal vasculature, controls substance exchange mainly via transportation processes between (paracellular) and through (transcellular) the retinal microvascular endothelium. Disruption of iBRB, characterized by retinal edema, is observed in many eye diseases and disturbs the physiological quiescence in the retina’s extracellular space, resulting in vision loss. Consequently, understanding the mechanisms of iBRB formation, maintenance, and breakdown is pivotal to discovering potential targets to restore function to compromised physiological barriers. These unraveled targets can also inform potential drug delivery strategies across the BRB and the blood–brain barrier into retinas and brain tissues, respectively. This review summarizes mechanistic insights into the development and maintenance of iBRB in health and disease, with a specific focus on the Wnt signaling pathway and its regulatory role in both paracellular and transcellular transport across the retinal vascular endothelium.
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KALLONIATIS, MICHAEL, GUIDO TOMISICH, JOHN W. WELLARD, and LISA E. FOSTER. "Mapping photoreceptor and postreceptoral labelling patterns using a channel permeable probe (agmatine) during development in the normal and RCS rat retina." Visual Neuroscience 19, no. 1 (January 2002): 61–70. http://dx.doi.org/10.1017/s0952523801191066.
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The aim of this study was to determine whether agmatine, a channel permeable probe, can identify photoreceptor dysfunction in the Royal College of Surgeons (RCS) retina at an earlier stage to that shown by apoptosis or anatomical markers, and also characterize the neurochemical development of the inner retina in the normal and degenerating rat. We used isolated retinas at different ages incubated in physiological media containing agmatine. Subsequently, postembedding immunocytochemistry was used to determine the number of labelled photoreceptors and the labelling pattern within postreceptoral neurons. Agmatine labelling patterns revealed a sequential development of retinal neurons beginning at postnatal day (PND)11/12 with most horizontal cells, a few ganglion and amacrine cells, showing a strong signal. The neurochemical development progressed rapidly, and reflects to a large part the known distribution of glutamate receptors, with inner nuclear labelling being evident by PND14, continuing with the same pattern of labelling in adulthood for the control retina. The RCS retina showed markedly reduced agmatine labelling in the inner retina at PND20. A rapid increase in photoreceptor AGB labelling was evident during the degeneration phase. Multiple samples at PND14 and PND16 confirmed a significant increase of labelled photoreceptors in the RCS retina.
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Cringle, S., D. Y. Yu, V. Alder, E. N. Su, and P. Yu. "Oxygen consumption in the avascular guinea pig retina." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 3 (September 1, 1996): H1162—H1165. http://dx.doi.org/10.1152/ajpheart.1996.271.3.h1162.
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Oxygen consumption across the retina of a mammal with a naturally avascular retina has not previously been investigated. The oxygen consumption across the avascular retina of the guinea pig was measured in vivo by spatial analysis of the intraretinal oxygen profile. The avascular nature of the guinea pig retina allows the inner retina to be included in the analysis without disrupting the normal physiological state of the retina. Oxygen-sensitive microelectrodes (1-micron tip) were used to make high-resolution measurements of oxygen tension through the retina of anesthetized, mechanically ventilated guinea pigs (n = 10). Oxygen profiles were then analyzed in terms of oxygen tension as a function of distance from the choriocapillaris/Bruch's membrane, and the data were fitted to an established mathematical model of retinal oxygen consumption. The average oxygen consumption of the full thickness of the guinea pig retina was 1.1 +/- 0.09 ml O2.min-1 x 100 g-1 (n = 10). The average oxygen consumption of the outer half of the retina was 2.07 +/- 0.17 ml O2.min-1 x 100 g-1, while that of the inner half was only 0.12 +/- 0.04 ml O2.min-1 x 100 g-1. A localized region of high oxygen consumption was identified in the outer retina in every case, and this region accounted for an average of 93.9 +/- 2.0% of the total retinal oxygen consumption. Only 5.2 +/- 1.4% of the total oxygen consumption was attributable to the inner half of the retina. When choroidal oxygen tension was increased via a combination of systemic hyperoxia and hypercapnia, high oxygen levels could be sustained in all retinal layers. Under these conditions of an excess oxygen supply, the inner retina still consumed only 0.45 +/- 0.11 ml O2.min-1 x 100 g-1, which was 13.8 +/- 2.5% of the total retinal oxygen consumed. The relatively low oxygen consumption in the inner retina of the guinea pig may reflect an interesting adaptation to the constraints imposed by the absence of a retinal circulation in this species.
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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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Walston, Steven T., Yao-Chuan Chang, James D. Weiland, and Robert H. Chow. "Method to remove photoreceptors from whole mount retina in vitro." Journal of Neurophysiology 118, no. 5 (November 1, 2017): 2763–69. http://dx.doi.org/10.1152/jn.00578.2017.
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Patch clamp recordings of neurons in the inner nuclear layer of the retina are difficult to conduct in a whole mount retina preparation because surrounding neurons block the path of the patch pipette. Vertical slice preparations or dissociated retinal cells provide access to bipolar cells at the cost of severing the lateral connection between neurons. We have developed a technique to remove photoreceptors from the rodent retina that exposes inner nuclear layer neurons, allowing access for patch clamp recording. Repeated application to and removal of filter paper from the photoreceptor side of an isolated retina effectively and efficiently removes photoreceptor cells and, in degenerate retina, hypertrophied Müller cell end feet. Live-dead assays applied to neurons remaining after photoreceptor removal demonstrated mostly viable cells. Patch clamp recordings from bipolar cells reveal responses similar to those recorded in traditional slice and dissociated cell preparations. An advantage of the photoreceptor peel technique is that it exposes inner retinal neurons in a whole mount retina preparation for investigation of signal processing. A disadvantage is that photoreceptor removal alters input to remaining retinal neurons. The technique may be useful for investigations of extracellular electrical stimulation, photoreceptor DNA analysis, and nonpharmacological removal of light input. NEW & NOTEWORTHY This study reports a method for removing photoreceptors from rodent whole mount retina while preserving the architecture of the inner retina. The method enables easier access to the inner retina for studies of neural processing, such as by patch clamp recording.
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HUANG, WEI, GUANGYU WU, and GUO-YONG WANG. "Cell type-specific and light-dependent expression of Rab1 and Rab6 GTPases in mammalian retinas." Visual Neuroscience 26, no. 5-6 (November 2009): 443–52. http://dx.doi.org/10.1017/s0952523809990277.
Full textAbstract:
AbstractThe Ras-like Rab1 and Rab6 GTPases modulate protein traffic along the early secretory pathway and are involved in the regulation of maturation of rhodopsin in the outer retina. However, Rab GTPases have not been studied in the inner retinas. Here, we analyzed the anatomatic distribution and expression of Rab1 and Rab6 in the mouse and rat retinas by immunohistochemistry and immunoblotting. We found that Rab1 was specifically expressed in the rod bipolar cells, while Rab6 was expressed in a different cell type(s) from rod bipolar cells in the inner retina. We also demonstrated that expression of Rab1 and Rab6 was increased with light. These data provided the first evidence implicating that Rab1 and Rab6 may be involved in the regulation of the retinal adaptation.
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Porrello, K., S. P. Bhat, and D. Bok. "Detection of interphotoreceptor retinoid binding protein (IRBP) mRNA in human and cone-dominant squirrel retinas by in situ hybridization." Journal of Histochemistry & Cytochemistry 39, no. 2 (February 1991): 171–76. http://dx.doi.org/10.1177/39.2.1987260.
Full textAbstract:
Interphotoreceptor retinoid binding protein (IRBP) is a soluble glycolipoprotein located between the neurosensory retina and pigment epithelium, which may serve to transport vitamin A derivatives between these tissues. The specific cell type responsible for IRBP synthesis has not been well established. To address this issue, we have examined the expression of IRBP mRNA in human and cone-dominant ground squirrel retinas by in situ hybridization. Optimal labeling and histological resolution were achieved with 35S- and 3H-labeled anti-sense riboprobes made from a human IRBP cDNA clone, and semi-thin wax-embedded retinal sections. In human retina, label was localized over the inner segments of both rod and cone photoreceptors. Quantitative analysis demonstrated a fourfold higher density of label over rod inner segments. In ground squirrel retina, labeling was found almost exclusively over the inner segments of cones. The results indicate that in human retina both rods and cones express IRBP mRNA, albeit at different levels. In cone-dominant species such as the ground squirrel, cones are the principal cell type responsible for IRBP mRNA synthesis.
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GRÜNDER, TATIANA, KONRAD KOHLER, and ELKE GUENTHER. "Alterations in NMDA receptor expression during retinal degeneration in the RCS rat." Visual Neuroscience 18, no. 5 (September 2001): 781–87. http://dx.doi.org/10.1017/s0952523801185111.
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To determine how a progressive loss of photoreceptor cells and the concomitant loss of glutamatergic input to second-order neurons can affect inner-retinal signaling, glutamate receptor expression was analyzed in the Royal College of Surgeons (RCS) rat, an animal model of retinitis pigmentosa. Immunohistochemistry was performed on retinal sections of RCS rats and congenic controls between postnatal (P) day 3 and the aged adult (up to P350) using specific antibodies against N-methyl-D-aspartate (NMDA) subunits. All NMDA subunits (NR1, NR2A–2D) were expressed in control and dystrophic retinas at all ages, and distinct patterns of labeling were found in horizontal cells, subpopulations of amacrine cells and ganglion cells, as well as in the outer and inner plexiform layer (IPL). NR1 immunoreactivity in the inner plexiform layer of adult control retinas was concentrated in two distinct bands, indicating a synaptic localization of NMDA receptors in the OFF and ON signal pathways. In the RCS retina, these bands of NR1 immunoreactivity in the IPL were much weaker in animals older than P40. In parallel, NR2B immunoreactivity in the outer plexiform layer (OPL) of RCS rats was always reduced compared to controls and vanished between P40 and P120. The most striking alteration observed in the degenerating retina, however, was a strong expression of NR1 immunoreactivity in Müller cell processes in the inner retina which was not observed in control animals and which was present prior to any visible sign of photoreceptor degeneration. The results suggest functional changes in glutamatergic receptor signaling in the dystrophic retina and a possible involvement of Müller cells in early processes of this disease.
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Wu, Zhi Long, and Zhi Jie Wang. "The Simulation of Retinal Inner Plexiform Layer Based on Parallel Algorithm." Advanced Materials Research 680 (April 2013): 509–14. http://dx.doi.org/10.4028/www.scientific.net/amr.680.509.
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The final objective of retinal simulation is to construct an artificial computer retina to replace the biological retina, and to offset the vision-impaired people. Due to the complexity of the retinal structure and the great number of bipolar cells and ganglion cells in retinal (exceeding tens of millions), both the speed and accuracy of the simulation of the retinal up to date are at a low level. In this paper we present a method for the simulation of inner plexiform layer of retina based on Compute Unified Device Architecture (CUDA) parallel algorithm to achieve the maximum utilization of CPU and Graphic Processing Unit(GPU), and to improve the speed and accuracy of the retina simulation.
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Vidal, M. N., Y. Segovia, N. Victory, A. Navarro-Sempere, and M. García. "Light Microscopy Study of the Retina of the Yellow-Legged Gull, Larus Michahellis, and the Relationship between Environment and Behaviour." Avian Biology Research 11, no. 4 (October 2018): 231–37. http://dx.doi.org/10.3184/175815618x15282819619105.
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The morphology of the retina of the adult Yellow-legged Gull, Larus michahellis, was examined in transverse sections under light microscopy in order to study the retinal adaptations to their specific photic environment that determines their behaviour. We identified rods, single cones and unequal double cones. Although it is a duplex retina, cones are preponderant and coloured oil droplets are present in their inner segments. As several colours in oil droplets are observed, it seems reasonable to conclude that several types of cones are present. Moreover, more cones per unit area are found in the central regions of the retina than in peripheral regions. A probable area centralis is observed. In the inner nuclear layer, two types of horizontal cells, and bipolar and amacrine cells can be recognised. Also, ganglion cells, characterised by prominent nuclei and nucleoli, vary in size and abundance among different regions in the retina. Comparisons are made with the retinae of other marine birds. The morphological characteristics of this retina indicate that Larus michahellis possesses: a good ability to discriminate colour; complex visual processing in the inner retina in order to mediate contrast and motion perception; and an elevated acuity in areas of high ganglion cell density.
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García-Ayuso, Diego, Johnny Di Pierdomenico, Manuel Vidal-Sanz, and María P. Villegas-Pérez. "Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration." International Journal of Molecular Sciences 20, no. 18 (September 19, 2019): 4649. http://dx.doi.org/10.3390/ijms20184649.
Full textAbstract:
Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina.
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Morera, Luis P., Nicolás M. Díaz, and Mario E. Guido. "Horizontal cells expressing melanopsin x are novel photoreceptors in the avian inner retina." Proceedings of the National Academy of Sciences 113, no. 46 (October 27, 2016): 13215–20. http://dx.doi.org/10.1073/pnas.1608901113.
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In the vertebrate retina, three types of photoreceptors—visual photoreceptor cones and rods and the intrinsically photosensitive retinal ganglion cells (ipRGCs)—converged through evolution to detect light and regulate image- and nonimage-forming activities such as photic entrainment of circadian rhythms, pupillary light reflexes, etc. ipRGCs express the nonvisual photopigment melanopsin (OPN4), encoded by two genes: the Xenopus (Opn4x) and mammalian (Opn4m) orthologs. In the chicken retina, both OPN4 proteins are found in ipRGCs, and Opn4x is also present in retinal horizontal cells (HCs), which connect with visual photoreceptors. Here we investigate the intrinsic photosensitivity and functioning of HCs from primary cultures of embryonic retinas at day 15 by using calcium fluorescent fluo4 imaging, pharmacological inhibitory treatments, and Opn4x knockdown. Results show that HCs are avian photoreceptors with a retinal-based OPN4X photopigment conferring intrinsic photosensitivity. Light responses in HCs appear to be driven through an ancient type of phototransduction cascade similar to that in rhabdomeric photoreceptors involving a G-protein q, the activation of phospholipase C, calcium mobilization, and the release of the inhibitory neurotransmitter GABA. Based on their intrinsic photosensitivity, HCs may have a key dual function in the retina of vertebrates, potentially regulating nonvisual tasks together with their sister cells, ipRGCs, and with visual photoreceptors, modulating lateral interactions and retinal processing.
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RICHARDS, ADAM, ALFRED A. EMONDI, and BAERBEL ROHRER. "Long-term ERG analysis in the partially light-damaged mouse retina reveals regressive and compensatory changes." Visual Neuroscience 23, no. 1 (January 2006): 91–97. http://dx.doi.org/10.1017/s0952523806231080.
Full textAbstract:
Most of the blinding retinopathies are due to progressive photoreceptor degeneration. Treatment paradigms that are currently being investigated include strategies to either halt or slow down photoreceptor cell loss, or to replace useful vision with retinal prosthesis. However, more information is required on the pathophysiological changes of the diseased retina, in particular the inner retina, that occur as a consequence of photoreceptor cell loss. Here we wished to use light damage as a stoppable insult to determine the structural and functional consequences on inner and outer retina, with the overall goal of determining whether survival of a functional inner retina is possible even if the outer retina is damaged. Mice were exposed to a 20-day light-damage period. Electroretinograms (ERG) and morphology were used to assess subsequent recovery. Outer retina was monitored analyzinga-waves, which represent photoreceptor cell responses, and histology. Integrity of the inner retina was monitored, analyzingb-waves and oscillatory potentials (OP1–OP4) and immunohistochemical markers for known proteins of the inner retina. All six ERG components were significantly suppressed with respect to amplitudes and kinetics, but stabilized in a wave-dependent manner within 40–70 days after the end of light exposure. As expected, damage of the outer retina was permanent. However, function of the inner retina was found to recover significantly. Whileb-wave amplitudes remained suppressed to 60% of their baseline values, OP amplitudes recovered completely, and implicit times of all components of the inner retina (b-wave and OP1–OP4) recovered to a level close to baseline values. Histological analyses confirmed the lack of permanent damage to the inner retina. In summary, these data suggests that the inner retina has the potential for significant recovery as well as plasticity if treatment is available to stop the deterioration of the outer retina.
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BURKHARDT, DWIGHT A. "Signals for color and achromatic contrast in the goldfish inner retina." Visual Neuroscience 31, no. 6 (June 5, 2014): 365–71. http://dx.doi.org/10.1017/s0952523814000157.
Full textAbstract:
AbstractA moving stimulus paradigm was designed to investigate color contrast encoding in the retina. Recently, this paradigm yielded suggestive evidence for color contrast encoding in zebrafish but the significance and generality remain uncertain since the properties of color coding in the zebrafish inner retina are largely unknown. Here, the question of color contrast is pursued in the goldfish retina where there is much accumulated evidence for retinal mechanisms of color vision and opponent color-coding, in particular. Recordings of a sensitive local field potential of the inner retina, the proximal negative response, were made in the intact, superfused retina in the light-adapted state. Responses to color contrast and achromatic contrast were analyzed by comparing responses to a green moving bar on green versus red backgrounds. The quantitative form of the irradiance/response curves was distinctly different under a range of conditions in 32 retinas, thereby providing robust evidence for red–green color contrast. The color contrast is based on successive contrast, occurs in the absence of overt color opponency, and clearly differs from previous findings in the goldfish retina for simultaneous color contrast mediated by color-opponent neurons. The form of the irradiance/response curves suggests that successive color contrast is particularly important when achromatic contrast is low, as often occurs in natural environments. The present results provide a parallel with the well-known principle of human color vision, first proposed by Kirschmann as the third law of color contrast, and may also have implications for the evolution of vertebrate color vision.
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GOTZES, SEBASTIAN, JAN de VENTE, and FRANK MÜLLER. "Nitric oxide modulates cGMP levels in neurons of the inner and outer retina in opposite ways." Visual Neuroscience 15, no. 5 (May 1998): 945–55. http://dx.doi.org/10.1017/s0952523898155141.
Full textAbstract:
In the mammalian retina, neuronal nitric oxide synthase (NOS) is mainly localized in subpopulations of amacrine cells. One function of nitric oxide (NO) is to stimulate soluble guanylate cyclases which in turn synthesize cGMP. We used an antibody specific for cGMP to demonstrate cGMP-like immunoreactivity (cG-IR) in bovine, rat, and rabbit retinae and investigated the effects on cGMP levels of both exogenously applied NO and of endogenously released NO. We found that cGMP levels in inner and outer retina were controlled in opposite ways. In the presence of the NO-donors SNP, SIN-1 or SNAP, cG-IR was prominent in neurons of the inner retina, mainly in cone bipolar cells, some amacrine and ganglion cells. Retinae incubated in IBMX showed weak cG-IR in bipolar cells. Glutamate increased cG-IR in the inner retina, presumably by stimulating endogenous NO release, whereas NOS inhibitors or GABA and glycine decreased cG-IR in bipolar cells by reducing NO release. In somata, inner segments and spherules of rod photoreceptors the situation was reversed. cG-IR was undetectable in the presence of NO-donors or glutamate, was moderate in IBMX-treated retinae, but increased strongly in the presence of NOS inhibitors or GABA/glycine. We conclude that NO is released endogenously in the retina. In the presence of NO, cGMP levels are increased in neurons of the inner retina, but are decreased in rods.
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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.
Full textAbstract:
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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Cohen, Bella, Manjeet Singh, Gaurav Gupta, Sean Savitz, Lenore C. Ocava, Pearl S. Rosenbaum, and Daniel M. Rosenbaum. "Death inducing ligands are critical for the selective vulnerability of the inner retina to transient global ischemia." Stroke 32, suppl_1 (January 2001): 352. http://dx.doi.org/10.1161/str.32.suppl_1.352-a.
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P72 We have previously demonstrated that the delayed cell death that occurs in the inner retina following transient global ischemia is in part apoptotic.In non-neuronal cells, death-inducing ligands(DILs) such as TNF-α and FasL are important in the induction of apoptosis.The purpose of this study was to investigate the role of DILs in the selective vulnerability of the inner retina to ischemic injury. Four groups of mice were subjected to transient global retinal ischemia (high intraocular pressure model) for a period of 45 minutes : wild type, TNFR(p55)-knock out, TNFR(p75)-knock out and lpr(loss of function of Fas receptor). The degree of retinal damage was assessed by measuring the thicknesses of the inner retinal layers. Additionally, electrophysiology (ERG) was performed following ischemia to assess functional outcome. There were TUNEL positive cells within the vulnerable inner retina seen maximally at 24 hours following ischemia. At 7 days subsequent to ischemia,in all groups of mice there was marked thinning of the inner retinal layers with morphological characterstics of apoptosis. ERG at 7 days demonstrated diminished amplitude of the ERG-b wave.In all three groups of mutant mice, there was significantly less morphological damage(mean inner retinal thickness) as well as significant preservation of the ERG-b wave as compared to the wild type animals.The lpr animals demonstrated the greatest protection.These data suggest that DILs play a critical role in the selective vulnerability of the inner retina to transient global ischemia and offer new strategies for the treatment of ischemic neuronal injury.
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HANZLICEK, BRETT W., NEAL S. PEACHEY, CHRISTIAN GRIMM, STEPHANIE A. HAGSTROM, and SHERRY L. BALL. "Probing inner retinal circuits in the rod pathway: A comparison of c-fos activation in mutant mice." Visual Neuroscience 21, no. 6 (November 2004): 873–81. http://dx.doi.org/10.1017/s0952523804216078.
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We have used wild-type mice and mice possessing defects in specific retinal circuits in order to more clearly define functional circuits of the inner retina. The retina of the nob mouse lacks communication between photoreceptors and depolarizing bipolar cells (DBCs). Thus, all light driven activity in the nob mouse is mediated via remaining hyperpolarizing bipolar cell (HBC) circuits. Transducin null (Trα−/−) mice lack rod photoreceptor activity and thus remaining retinal circuits are solely generated via cone photoreceptor activity. Activation in inner retinal circuits in each of these mice was identified by monitoring light-induced expression of an immediate early gene, c-fos. The number of cells expressing c-fos in the inner retina was dependent upon stimulus intensity and was altered in a systematic fashion in mice with known retinal mutations. To determine whether c-fos is activated via circuits other than photoreceptors in the outer retina, we examined c-fos expression in tulp1−/− mice that lack photoreceptors in the outer retina; these mice showed virtually no c-fos activity following light exposure. Double-labeling immunohistochemical studies were carried out to more clearly define the population of c-fos expressing amacrine cells. Our results indicate that c-fos may be used to map functional circuits in the retina.
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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.
Full textAbstract:
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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Ma, Guangying, Jie Ding, Tae-Hoon Kim, and Xincheng Yao. "Quantitative Optical Coherence Tomography for Longitudinal Monitoring of Postnatal Retinal Development in Developing Mouse Eyes." Applied Sciences 12, no. 4 (February 11, 2022): 1860. http://dx.doi.org/10.3390/app12041860.
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A better study of postnatal retinal development is essential for the in-depth understanding of the nature of the vision system. To date, quantitative analysis of postnatal retinal development is primarily limited to endpoint histological examination. This study is to validate in vivo optical coherence tomography (OCT) for longitudinal monitoring of postnatal retinal development in developing mouse eyes. OCT images of C57BL/6J mice were recorded from postnatal day (P) 14 to P56. Three-dimensional (3D) frame registration and super averaging were adopted to investigate the fine structure of the retina. Quantitative OCT analysis revealed distinct outer and inner retinal layer changes, corresponding to eye development. At the outer retina, external limiting membrane (ELM) and ellipsoid zone (EZ) band intensities gradually increased with aging, and the IZ band was detectable by P28. At the inner retina, a hyporeflective layer (HRL) between the nerve fiber layer (NFL) and inner plexiform layer (IPL) was observed in developing eyes and gradually disappeared with aging. Further image analysis revealed individual RGCs within the HRL layer of the young mouse retina. However, RGCs were merged with the NFL and the IPL in the aged mouse retina. Moreover, the sub-IPL layer structure was observed to be gradually enhanced with aging. To interpret the observed retinal layer kinetics, a model based on eyeball expansion, cell apoptosis, and retinal structural modification was proposed.
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Liu, Hanhan, and Verena Prokosch. "Energy Metabolism in the Inner Retina in Health and Glaucoma." International Journal of Molecular Sciences 22, no. 7 (April 1, 2021): 3689. http://dx.doi.org/10.3390/ijms22073689.
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Glaucoma, the leading cause of irreversible blindness, is a heterogeneous group of diseases characterized by progressive loss of retinal ganglion cells (RGCs) and their axons and leads to visual loss and blindness. Risk factors for the onset and progression of glaucoma include systemic and ocular factors such as older age, lower ocular perfusion pressure, and intraocular pressure (IOP). Early signs of RGC damage comprise impairment of axonal transport, downregulation of specific genes and metabolic changes. The brain is often cited to be the highest energy-demanding tissue of the human body. The retina is estimated to have equally high demands. RGCs are particularly active in metabolism and vulnerable to energy insufficiency. Understanding the energy metabolism of the inner retina, especially of the RGCs, is pivotal for understanding glaucoma’s pathophysiology. Here we review the key contributors to the high energy demands in the retina and the distinguishing features of energy metabolism of the inner retina. The major features of glaucoma include progressive cell death of retinal ganglions and optic nerve damage. Therefore, this review focuses on the energetic budget of the retinal ganglion cells, optic nerve and the relevant cells that surround them.
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MENSINGER, ALLEN F., and MAUREEN K. POWERS. "Visual function in regenerating teleost retina following cytotoxic lesioning." Visual Neuroscience 16, no. 2 (March 1999): 241–51. http://dx.doi.org/10.1017/s0952523899162059.
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Teleost fish retinas can regenerate in vivo in adulthood. Retinal and visual function was assessed in adult goldfish following comprehensive retinal destruction by intraocular injection of ouabain. Electroretinograms (ERGs) and the dorsal light reflex (DLR) were used to evaluate the return of visual function. ERGs were detectable in regenerating eyes 50 to 70 days following ouabain injection. Amplitudes of both a- and b-waves increased steadily through day 210 following ouabain treatment, at which time a-wave amplitude was 90% and b-wave amplitude approached 50% of the contralateral control eye. The progressive gain observed in the a-wave was attributed to photoreceptor regeneration. The increase in b-wave amplitude was attributed to an increase in the number of inner nuclear layer cells and the number and efficacy of neuronal connections to or within the inner retina. The photopic spectral sensitivity of the b-wave in regenerating retina closely matched the intrafish control retina, suggesting that the relative numbers of cone photoreceptors was normal in regeneration. The recovery of the DLR (indicated by improved postural balance during regeneration) paralleled electrophysiological gains during retinal regeneration. Fish displayed a marked longitudinal body imbalance toward the control eye following retinal destruction. Improvement in equilibrium was correlated with increasing b-wave amplitudes. When the b-wave reached 50% of control amplitude (30 weeks), normal posture was restored. The return of the ERG indicates that photoreceptors and their synaptic connections must be functional in regenerating retina. Failure of the retina to regenerate produced an abnormal DLR that persisted through 30 weeks and ERGs were not measurable. The return of normal equilibrium indicates that the regenerating retina can establish central connections to the brain, and that the regenerated connections can mediate functional visual behavior.
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Singh, Ankur, Preeti Diwaker, Akanksha Agrawal, Aniruddha Agarwal, Jolly Rohatgi, Ramandeep Singh, Gopal Krushna Das, Pramod Kumar Sahoo, and Vinod Kumar Arora. "Spectral Domain Optical Coherence Tomography Findings in Vision-Threatening Rhino-Orbital Cerebral Mucor Mycosis—A Prospective Analysis." Diagnostics 12, no. 12 (December 8, 2022): 3098. http://dx.doi.org/10.3390/diagnostics12123098.
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Rhino-orbital cerebral mucor mycosis is a rare disease entity, where retinal involvement is described in the literature mostly as CRAO. However, pathological studies have shown mucor invading the choroid and retina with a neutrophilic reaction. So, it is pertinent that retinal inflammation secondary to invading mucor has some role in microstructural changes seen in the vitreous and retina of these patients. This novel study aims to describe the vitreal and retinal features of patients with vision-threatening rhino-orbital cerebral mucor mycosis and how they evolve on spectral domain optical coherence tomography (SD-OCT). This study shall also provide insight into the pathophysiology of these vitreoretinal manifestations by in vitro analysis of the exenterated orbital content. Fifteen eyes of fifteen patients with vision-threatening ROCM treated with standard care were enrolled in this study and underwent complete ophthalmic examination, serial colour fundus photography, and SD-OCT for both qualitative and quantitative analysis, at baseline and follow-up visits. SD-OCT on serial follow-up revealed thickening and increased inner-retinal reflectivity at presentation followed by thinning of both, other features such as the loss of the inner-retinal organized layer structure, external limiting membrane (ELM) disruption, necrotic spaces in the outer retina, and hyperreflective foci. Vitreous cells with vitreous haze were also seen. There was a significant reduction in CMT, inner and outer retinal thickness, total retinal thickness (all p < 0.05) with time, the quantum of reduction concentrated primarily to the inner retina. In summary, in vivo and in vitro analysis revealed that early microstructural changes were primarily a result of retinal infarctions secondary to thrombotic angioinvasion. With the late microstructural changes, there was possible sequelae of retinal infarction with some contribution from the inflammation, resulting from mucor invading the choroid and retina.
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CAO, QI-LIN, HEATHER A. MURPHY, and HEYWOOD M. PETRY. "Localization of nitric oxide synthase in the tree shrew retina." Visual Neuroscience 16, no. 3 (May 1999): 399–409. http://dx.doi.org/10.1017/s0952523899163016.
Full textAbstract:
Nitric oxide (NO) is a novel neuronal messenger that likely influences retinal function by activating retinal guanylyl cyclase to increase levels of cGMP. In the present study, the localization of neuronal nitric oxide synthase (nNOS, Type I NOS) in the cone-dominant tree shrew retina was studied using NADPH-d histochemistry and nNOS immunocytochemistry. Both NADPH-d and nNOS-immunoreactivity (IR) labeled the inner segments of rods and the myoids of a regular subpopulation of cones, with their corresponding nuclei outlined. The labeled cone myoids were co-localized with a marker for short-wave-sensitive (SWS) cones (S-antigen) and also displayed the regular triangular packing and density (7%) characteristic of SWS cones in tree shrew and other mammalian retinas. These measures confirmed the identity of the labeled cones as SWS cones. Photoreceptor ellipsoids of all cones were strongly labeled by NADPH-d reactivity, but lacked nNOS-IR. Another novel finding in tree shrew retina was that both NADPH-d and nNOS-IR labeled Müller cells, which have not been labeled by nNOS-IR in other mammalian retinas. Consistent with findings in rod-dominant retinas, two types of amacrine cells at the vitreal edge of the inner nuclear layer and a subpopulation of displaced amacrine cells at the scleral edge of the ganglion cell layer were labeled by both NADPH-d and nNOS-IR. Processes of these labeled cells were seen to extend into the inner plexiform layer, where dense punctate label was seen, especially in the central sublamina. These results show that localization of NOS in the cone-dominant tree shrew retina shares some common properties with rod-dominant mammalian retinas, but also shows some species-specific characteristics. The new finding of nNOS localization in tree shrew SWS cones and rods, but not in other cones, raises interesting questions about the roles of NO in the earliest level of visual processing.
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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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Linberg, Kenneth A., and Steven K. Fisher. "A burst of differentiation in the outer posterior retina of the eleven-week human fetus: An ultrastructural study." Visual Neuroscience 5, no. 1 (July 1990): 43–60. http://dx.doi.org/10.1017/s0952523800000067.
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AbstractMany studies on human retinal development have cited the third gestational month as a period when the posterior retina undergoes rapid differentiation and maturation, including a lining up of cone precursors. Ultrastructural data on the posterior retina during the third month are very limited, and totally lacking for the cone monolayer. We have examined two human fetal retinas between ten and 11 gestational weeks. Before the appearance of the cone monolayer, the outer neural retina consists of a homogeneous population of undifferentiated neuroblasts. Mitotic figures are still evident, even posteriorally. There is no outer plexiform layer (OPL). The interface of neural retina to retinal pigment epithelium (RPE) is largely featureless. By 11 weeks, the posterior retina has a thin OPL that separates the many rows of cells in the developing inner nuclear layer from the single tier of macular cone precursors. The RPE monolayer consists of cuboidal cells whose apical surface elaborates ridges of cytoplasm and branched processes that project into the subretinal space. The large, cuboidal cones are linked to each other and Müller cells at the outer limiting membrane. They show definitive signs of the structural polarity typical of vertebrate photoreceptors. Their apical cytoplasm contains many organelles common to the inner segment, while the basal cytoplasm has synaptic ribbons and vesicles, and receives invaginating contacts from processes in the OPL neuropil arising from differentiating second-order neurons. Lateral cone surfaces are mutually underlain by large subsurface cisterns.
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Mitori, Hikaru, Takeshi Izawa, Mitsuru Kuwamura, Masahiro Matsumoto, and Jyoji Yamate. "Developing Stage-dependent Retinal Toxicity Induced by l-glutamate in Neonatal Rats." Toxicologic Pathology 44, no. 8 (November 15, 2016): 1137–45. http://dx.doi.org/10.1177/0192623316676424.
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The neurotransmitter glutamate causes excitotoxicity in the human retina. In neonatal rats, the degree of glutamate-induced retinal damage depends on age at administration. To elucidate the sensitivity to glutamate on various developing stage of retina, we investigated glutamate-induced retinal damage and glutamate target cells on each postnatal day (PND). Newborn rats received a single subcutaneous administration of l-glutamate on PNDs 1 to 14. Retinal cell apoptosis characterized as pyknotic and terminal deoxynucleotidyl transferase–mediated dUTP digoxigenin nick end labeling–positive nuclei was analyzed at 6 hr after treatment, and sequential morphological features of retina were evaluated on PND 21. The inner retina on PND 21 exhibited thinning in rats treated after PND 2. The thinning was most severe in rats treated on PND 8 and the number of apoptotic cells also peaked. No thinning was observed in rats treated on PND 14. In the inner nuclear layer, glutamate target cells were mainly amacrine cells; additionally, bipolar cells and horizontal cells were damaged on PND 8. These retinal changes were more severe in central retina than those in peripheral retina on PND 8. Our findings indicate the morphological consequences of glutamate-induced retinal excitotoxicity and glutamate target cells on each PND and reveal that glutamate-induced retinal damage depends on developing stage.
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Silveira, L. C. L., E. S. Yamada, and C. W. Picanço-Diniz. "Displaced horizontal cells and biplexiform horizontal cells in the mammalian retina." Visual Neuroscience 3, no. 5 (November 1989): 483–88. http://dx.doi.org/10.1017/s0952523800005988.
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AbstractWe have used the neurofibrillar method of Gros-Schultze to stain the axonless horizontal cells of capybara, agouti, cat, and rabbit retinae. In all of these species, we have found two unusual horizontal cell morphologies: displaced horizontal cells and biplexiform horizontal cells. The displaced horizontal cells have perikarya located in the ganglion cell layer and dendrites branching in the inner plexiform layer. Many dendrites take an ascending trajectory to branch in the outer plexiform layer. The biplexiform horizontal cells are normally placed horizontal cells with descending processes that branch in the inner plexiform layer. Both cell types occur mainly in the retinal periphery, near the ora serrata. They are more numerous in the capybara retina, where they represent as much as 50% of the axonless horizontal cells of the retinal periphery.
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RENTERÍA, RENÉ C., EMANUEL E. STREHLER, DAVID R. COPENHAGEN, and DAVID KRIZAJ. "Ontogeny of plasma membrane Ca2+ ATPase isoforms in the neural retina of the postnatal rat." Visual Neuroscience 22, no. 3 (May 2005): 263–74. http://dx.doi.org/10.1017/s0952523805223027.
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Calcium ion (Ca2+) signaling has been widely implicated in developmental events in the retina, but little is known about the specific mechanisms utilized by developing neurons to decrease intracellular Ca2+. Using immunocytochemistry, we determined the expression profiles of all known isoforms of a key Ca2+ transporter, the plasma membrane Ca2+ ATPase (PMCA), in the rat retina. During the first postnatal week, the four PMCA isoforms were expressed in patterns that differed from their expression in the adult retina. At birth, PMCA1 was found in the ventricular zone and nascent cell processes in the distal retina as well as in ganglion and amacrine cells. After the first postnatal week, PMCA1 became restricted to photoreceptors and cone bipolar cells. By P10 (by postnatal day 10), most inner retinal PMCA consisted of PMCA2 and PMCA3. Prominent PMCA4 expression appeared after the first postnatal week and was confined primarily to the ON sublamina of the inner plexiform layer (IPL). The four PMCA isoforms could play distinct functional roles in the development of the mammalian retina even before synaptic circuits are established. Their expression patterns are consistent with the hypothesis that inner and outer retinal neurons have different Ca2+ handling needs.
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Gregory, Meredith, Emily Whiston, Norito Sugi, Coralynn Sack, Merideth C. Kamradt, Susan Heimer, Michael S. Gilmore, and Bruce R. Ksander. "αB-crystallin protects the retina during S. aureus induced endophthalmitis (45.2)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S57. http://dx.doi.org/10.4049/jimmunol.178.supp.45.2.
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Abstract Purpose: Bacterial infections in the posterior of the eye (endophthalmitis) result in toxin-related retinal destruction. However, it is not known whether apoptosis contributes to infection pathology. We are investigating whether αB-crystallin protects retinal tissue during S. aureus endophthalmitis. αB-crystallin is an anti-apoptotic small heat shock protein constitutively expressed in the retina. We hypothesize that αB-crystallin protects the retina from apoptosis. Methods: 129S6/SvEv αB-crystallin KO and wild-type mice received intravitreal injections of 500 CFU S. aureus. Clinical examinations and ERGs (electroretinalgram) were performed at 24, 48, 72 and 96 hours. Eyes were analyzed histologically for apoptosis via TUNEL staining. Results: Infected WT mice had only low levels of apoptosis in the inner nuclear layer of the retina. By contrast, infected KO mice displayed: decreased ERG retinal function,increased retinal destruction via histopathology, andhigher levels of apoptosis in the ganglion cell, inner nuclear and outer nuclear retinal layers at 48 hours. Further experiments demonstrated that S. aureus triggers up-regulation of αB-crystallin in the retina andS. aureus produces a protease that cleaves and inactivates αB-crystallin in vitro and in vivo. Conclusions: Bacterial-induced apoptosis of the retina occurs during endophthalmitis. αB-crystallin is increased to prevent retinal apoptosis, while bacterial proteases are released in an attempt to invade the retina. NIH-EY-016145 (M Gregory)
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Fusz, Katalin, Tamás Kovács-Öller, Péter Kóbor, Edina Szabó-Meleg, Béla Völgyi, Péter Buzás, and Ildikó Telkes. "Regional Variation of Gap Junctional Connections in the Mammalian Inner Retina." Cells 10, no. 9 (September 12, 2021): 2396. http://dx.doi.org/10.3390/cells10092396.
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The retinas of many species show regional specialisations that are evident in the differences in the processing of visual input from different parts of the visual field. Regional specialisation is thought to reflect an adaptation to the natural visual environment, optical constraints, and lifestyle of the species. Yet, little is known about regional differences in synaptic circuitry. Here, we were interested in the topographical distribution of connexin-36 (Cx36), the major constituent of electrical synapses in the retina. We compared the retinas of mice, rats, and cats to include species with different patterns of regional specialisations in the analysis. First, we used the density of Prox1-immunoreactive amacrine cells as a marker of any regional specialisation, with higher cell density signifying more central regions. Double-labelling experiments showed that Prox1 is expressed in AII amacrine cells in all three species. Interestingly, large Cx36 plaques were attached to about 8–10% of Prox1-positive amacrine cell somata, suggesting the strong electrical coupling of pairs or small clusters of cell bodies. When analysing the regional changes in the volumetric density of Cx36-immunoreactive plaques, we found a tight correlation with the density of Prox1-expressing amacrine cells in the ON, but not in the OFF sublamina in all three species. The results suggest that the relative contribution of electrical synapses to the ON- and OFF-pathways of the retina changes with retinal location, which may contribute to functional ON/OFF asymmetries across the visual field.
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Pan, B. X., K. M. Yee, F. N. Ross-Cisneros, A. A. Sadun, and J. Sebag. "Inner Retinal Optic Neuropathy: Vitreomacular Surgery-Associated Disruption of the Inner Retina." Investigative Ophthalmology & Visual Science 55, no. 10 (September 18, 2014): 6756–64. http://dx.doi.org/10.1167/iovs.14-15235.
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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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SPRINGER, A. D., and A. E. HENDRICKSON. "Development of the primate area of high acuity, 3: Temporal relationships between pit formation, retinal elongation and cone packing." Visual Neuroscience 22, no. 2 (March 2005): 171–85. http://dx.doi.org/10.1017/s095252380522206x.
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By establishing an avascular, highly elastic, region within the fetal area of high acuity (AHA), the developing primate eye has created a unique substrate on which the mechanical forces of intraocular pressure (IOP) and growth-induced retinal stretch (stretch) can act. We proposed (Springer & Hendrickson, 2004b) that these forces generate both the pit and high cone density found in the adult AHA. In this paper, we use quantitative measures to determine the temporal relationships between nasal and temporal retinal elongation, changes in pit depth, cone packing, and cone morphology over M. nemestrina retinal development. Retinal length increased rapidly to about 105 days postconception (dpc; Phase 1) and then elongation virtually ceased (Phase 2) until just after birth (180 dpc). Retinal elongation due to stretch resumed during Phase 3 until approximately 315 dpc (4–5 months), after which time the retina appeared mature (Phase 4). The pit appeared during the quiescent Phase 2, suggesting that IOP acts, in conjunction with molecular changes in the inner retina, on the highly elastic, avascular, AHA to generate a deep, narrow pit and causes inner retinal cellular displacements. Subsequently (Phase 3), the pit widened, became 50% shallower and central inner retinal lamina thinned slightly due to a small amount of retinal stretch occurring in the AHA. Centripetal movement of cones was minimal until just after birth when the pit reached 88% of its maximal depth. Accelerated cone packing during Phase 3 was temporally correlated with increased stretch. A slight stretching of the central inner retina generates “lift” forces that cause the pit to become shallower and wider. In turn, these “lift” forces draw cones toward the center of the AHA (Springer, 1999). Localized changes in cone morphology associated with packing, included smaller cell body size, a change from a monolayer to a multilayered mound of cell bodies, elongation of inner segments and tilting of the apical portion toward the AHA. These changes began in cones overlying the edges of the pit, not its center. Henle cone axons formed initially in association with centrifugal displacement of the inner retina during pit formation, with an additional subsequent elongation due to cones moving centripetally. An integrated, two-factor model of AHA formation is presented. Initially, during the second half of gestation (Phase 2), IOP acts on the hyperelastic avascular zone of the AHA to generate a deep pit in the inner retina. In the first 4 months after birth (Phase 3), central retinal stretch generates tensile “lift” forces that remodel the pit and pack cones by drawing them toward the AHA center.
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Alix, Belén, Yolanda Segovia, and Magdalena García. "The Structure of the Retina of the Eurasian Eagle-Owl and its Relation to Lifestyle." Avian Biology Research 10, no. 1 (February 2017): 36–44. http://dx.doi.org/10.3184/175815617x14799886573147.
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The retinal layers of birds are the same as those of other vertebrates; however, some variations exist in morphology, areas of visual acuity, and retinal vascularisation. Moreover, as a result of the relationship between environment, visual perception and behaviour, some variations are observed between diurnal and nocturnal birds. In this study, we have investigated the retina of the Eurasian Eagle-owl ( Bubo bubo hispanicus) by optical microscopy. The results indicate that the retina has features of both nocturnal and diurnal birds. The pigment epithelium cells have long prolongations filled with melanin granules. The rod is the dominant photoreceptor, but simple cones are abundant. Yellow and colourless oil droplets and paraboloid are present in the inner segment of cones. In the inner nuclear layer, the cell bodies of horizontal cells can easily be recognised by a large and pale cytoplasm. Bipolar cell perikarya are identified by their dark nuclei and the round and narrow cytoplasm. Amacrine cells, located in the inner border of the inner nuclear layer, have a round perikarya and lightly stained nuclei. Müller cells bodies, also located in this region, have an irregular shape. Finally, ganglion cells which are characterised by the prominent nuclei and nucleoli vary in size and abundance depending on different regions in the retina. The morphological characteristics of this retina indicate that B. b. hispanicus have a high light sensitivity, the capacity to discriminate colour, a complex visual processing in the inner retina in order to mediate contrast and motion and, possibly, an elevated acuity in areas of high photoreceptor and ganglion cell density.
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Mathew, Biji, Leianne A. Torres, Lorea Gamboa Acha, Sophie Tran, Alice Liu, Raj Patel, Mohansrinivas Chennakesavalu, et al. "Uptake and Distribution of Administered Bone Marrow Mesenchymal Stem Cell Extracellular Vesicles in Retina." Cells 10, no. 4 (March 25, 2021): 730. http://dx.doi.org/10.3390/cells10040730.
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Cell replacement therapy using mesenchymal (MSC) and other stem cells has been evaluated for diabetic retinopathy and glaucoma. This approach has significant limitations, including few cells integrated, aberrant growth, and surgical complications. Mesenchymal Stem Cell Exosomes/Extracellular Vesicles (MSC EVs), which include exosomes and microvesicles, are an emerging alternative, promoting immunomodulation, repair, and regeneration by mediating MSC’s paracrine effects. For the clinical translation of EV therapy, it is important to determine the cellular destination and time course of EV uptake in the retina following administration. Here, we tested the cellular fate of EVs using in vivo rat retinas, ex vivo retinal explant, and primary retinal cells. Intravitreally administered fluorescent EVs were rapidly cleared from the vitreous. Retinal ganglion cells (RGCs) had maximal EV fluorescence at 14 days post administration, and microglia at 7 days. Both in vivo and in the explant model, most EVs were no deeper than the inner nuclear layer. Retinal astrocytes, microglia, and mixed neurons in vitro endocytosed EVs in a dose-dependent manner. Thus, our results indicate that intravitreal EVs are suited for the treatment of retinal diseases affecting the inner retina. Modification of the EV surface should be considered for maintaining EVs in the vitreous for prolonged delivery.