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At least 433 records · Page 24Linked to original sources
PubMed2002

Retinal detachment in developing countries.

Treatment of retinal detachment has been a low priority in developing countries. It is thought to be less common in India and Africa than in Europe and N America. The aetiology and presentation of retinal detachment in the Third World are affected by genetic and environmental factors. In general, patients are more likely to present late, and complex detachments are relatively more common. Despite these problems, the results of surgery are encouraging, with more than 80% final anatomical success, and over 60% of re-attached retinas obtaining vision of 6/60 or better. The management of retinal detachment in developing countries can be improved by strengthening training programmes and by developing and equipping centres to carry out retinal surgery.

Developing Countries↗
PubMed1998

New developments in retinal drusen.

Retinal drusen are an important manifestation of age-related maculopathy, and increase with ageing. Recent studies have shown that gentle laser photocoagulation can lead to resolution of soft drusen and may lessen the high risk of development of choroidal neovascularisation in these cases. Laser induced regression of retinal drusen appears to be a safe technique, but no long term results are yet available. Retinal drusen may also occur as a dominantly inherited disorder and current evidence suggests that these represent more than one disorder. Misclassification of retinal drusen as retinal exudates is an important cause of false positive referral in diabetic retinopathy screening programmes.

Aged↗
PubMed1999

Spontaneous activity in developing turtle retinal ganglion cells: pharmacological studies.

Extracellular recordings were obtained from the ganglion cell (GC) layer during correlated spontaneous bursting activity (SBA) in the immature turtle retina. Pharmacological agents were bath-applied, and their effects on burst and correlation parameters were determined. SBA requires synaptic transmission. It was blocked in the presence of curare and mecamylamine, two cholinergic nicotinic antagonists, and enhanced with neostigmine, a cholinesterase inhibitor. SBA was profoundly inhibited during blockade of glutamatergic receptors with the broad spectrum antagonist kynurenate and it vanished with 6,7-dinitroquinoxaline-2-3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), two AMPA/kainate receptor antagonists. Blockade of NMDA receptors with D(-)-2-amino-5-phosphonopentanoic acid (D-AP-5) led only to a modest reduction in SBA. Blockade of GABAA receptors with bicuculline prolonged the duration of the bursts. Inhibition of GABA uptake with nipecotic acid led to a decrease in burst rate. Blockade of K+ channels with cesium (Cs+) and tetraethylammonium (TEA) led to a dramatic decrease in excitability. Burst propagation between neighboring GCs was reduced by K+ channel blockade. Gap junction blockade had no consistent effect on bursts or correlation parameters. None of these drugs had a strong effect on the refractory period between bursts. We conclude that correlated SBA in immature turtle GCs requires both cholinergic nicotinic and glutamatergic (mainly through AMPA/kainate receptors) synaptic transmission. GABAergic activity modulates the intensity and the duration of the bursts. Extracellular K+ is involved in lateral activity propagation and increases retinal excitability, which may be required for burst generation.

Action Potentials↗
PubMed1993

Molecular cloning of the murine JAK1 protein tyrosine kinase and its expression in the mouse central nervous system.

Degenerate oligonucleotide primers were employed in PCRs to clone protein tyrosine kinases that may play potential roles in the development of the mammalian CNS. Using one PCR clone to screen a mouse eye cDNA library, a full-length cDNA of a cytoplasmic tyrosine kinase, the homolog of human JAK1, was obtained. The murine JAK1 kinase belongs to a new family of cytoplasmic kinases that contain two tandem catalytic domains. Northern analyses indicated that murine JAK1 mRNA is expressed in a variety of tissues and cell lines. In the adult mouse eye, in situ hybridization and immunohistochemistry showed that JAK1 mRNA and protein were expressed in the retinal ganglion cell layer and the inner part of the inner nuclear layer, presumably in amacrine cells. JAK1 protein was also detected in horizontal cells and in the two synaptic layers of the adult retina. During retinal development, JAK1 protein was first detected in retinal ganglion cells and in their axons as early as embryonic day 14. Expression of JAK1 protein in amacrine cells and horizontal cells occurred only postnatally. This pattern of expression was also observed in the chick retina, suggesting an evolutionarily conserved function of JAK1 kinase in vertebrate retinal development and/or function. Immunohistochemical staining against JAK1 was detected in two areas of the adult mouse brain, the olfactory bulb and a group of cells in the hypothalamus. Together, these expression studies suggest a role for JAK1 kinase in the differentiation or function of a subset of CNS neurons.

Aging↗
PubMed2003

Characterization of Wnt signaling components and activation of the Wnt canonical pathway in the murine retina.

The neuroepithelial layer of the developing eyecup contains multipotential precursor cells that give rise to all of the neurons and the one glial cell type present in the adult retina. Patterning within the retinal neuroepithelium is regulated by cell intrinsic as well as cell extrinsic mechanisms. Although the identity of some of the signaling molecules that regulate retinal development is known, the function of many others, especially members of the Wnt family, has yet to be characterized in the context of retinal development. We undertook a comprehensive in situ hybridization analysis to examine the expression of Wnt pathway components in the developing and adult mouse neural retina. Our findings confirm and extend previous expression studies in mice and other vertebrates, as we show that Wnt-3, -5a, -5b, and -7b are expressed in the neural retina and that there is a dynamic pattern of Wnt receptor (Mouse frizzled [Mfz]) and Wnt antagonist (Secreted-frizzled-related protein [Sfrp]) gene expression in the embryonic and perinatal neural retina. Moreover, we show that Wnt-13 is expressed in the pigment epithelium overlying the distal part of the eyecup and the ciliary margin and that Mfz-4, -6, and -7 are expressed in different regions within the ciliary margin. To determine where activation of canonical Wnt signaling is occurring in the retina, we examined reporter gene expression in TCF/Lef-LacZ mice and we demonstrate that the highest levels of beta-gal activity are found in the ciliary margin, adjacent to and within the Wnt-13 expression domain, implicating Wnt-13 signaling in the development of the ciliary margin and its derivatives.

Animals↗
PubMed1985

Development of retinal neovascularisation in vascular occlusive disease.

Retinal neovascularisation in 80 non-diabetic patients with occlusive retinal vascular disease appeared to be related at least as frequently to arterial as to venous occlusive disease. Intraretinal, preretinal and prepapillary neovascularisation had developed in 76 per cent, 47 per cent and 49 per cent respectively of the specimens. Neovascularisation in the adult retina is thought to develop in the following sequence of histopathologic features: plasmatic insudation and transudation of the vessel walls (100 per cent of the specimens), endothelial cell proliferation (97 per cent) and capillary formation (76 per cent). Intramural newly-formed capillaries in thickened hyalinized vessels were observed in 68 per cent of the specimens. Not only retinal vein occlusion but also slowly progressive arterial and arteriolar occlusive diseases may produce retinal neovascularisation, originating from arterioles, venules and capillaries which are involved in a hypoxic degenerative endothelial process which gives rise to endothelial proliferation.

Aged↗
PubMedDate not supplied

In vivo development of retinal ON-bipolar cell axonal terminals visualized in nyx::MYFP transgenic zebrafish.

Axonal differentiation of retinal bipolar cells has largely been studied by comparing the morphology of these interneurons in fixed tissue at different ages. To better understand how bipolar axonal terminals develop in vivo, we imaged fluorescently labeled cells in the zebrafish retina using time-lapse confocal and two photon microscopy. Using the upstream regulatory sequences from the nyx gene that encodes nyctalopin, we constructed a transgenic fish in which a subset of retinal bipolar cells express membrane targeted yellow fluorescent protein (MYFP). Axonal terminals of these YFP-labeled bipolar cells laminated primarily in the inner half of the inner plexiform layer, suggesting that they are likely to be ON-bipolar cells. Transient expression of MYFP in isolated bipolar cells indicates that two or more subsets of bipolar cells, with one or two terminal boutons, are labeled. Live imaging of YFP-expressing bipolar cells in the nyx::MYFP transgenic fish at different ages showed that initially, filopodial-like structures extend and retract from their primary axonal process throughout the inner plexiform layer (IPL). Over time, filopodial exploration becomes concentrated at discrete foci prior to the establishment of large terminal boutons, characteristic of the mature form. This sequence of axonal differentiation suggests that synaptic targeting by bipolar cell axons may involve an early process of trial and error, rather than a process of directed outgrowth and contact. Our observations represent the first in vivo visualization of axonal development of bipolar cells in a vertebrate retina.

Animals↗
PubMed1984

An extracellular retinol-binding glycoprotein in the eyes of mutant rats with retinal dystrophy: development, localization, and biosynthesis.

Interstitial retinol-binding protein (IRBP) is a soluble glycoprotein in the interphotoreceptor matrix of bovine, human, monkey, and rat eyes. It may transport retinol between the retinal pigment epithelium and the neural retina. In light-reared Royal College of Surgeons (RCS) and RCS retinal dystrophy gene (rdy)+ rats, the amount of IRBP in the interphotoreceptor matrix increased in corresponding proportion to the amount of total rhodopsin through postnatal day 22 (P22). In the RCS-rdy+ rats, the amount increased slightly after P23. However, in the RCS rats there was a rapid fall in the quantity of IRBP as the photoreceptors degenerated between P23 and P29. No IRBP was detected by immunocytochemistry in rats at P28. The amount of rhodopsin fell more slowly. Although retinas from young RCS and RCS-rdy+ rats were able to synthesize and secrete IRBP, this ability was lost in retinas from older RCS rats (P51, P88) but not their congenic controls. The photoreceptor cells have degenerated at these ages in the RCS animals, and may therefore be the retinal cells responsible for IRBP synthesis. The putative function of IRBP in the extracellular transport of retinoids during the visual cycle is consistent with a defect in retinol transport in the RCS rat reported by others.

Aging↗
PubMed2005

Molecular cloning of three zebrafish lin7 genes and their expression patterns in the retina.

The vertebrate retina develops from an undifferentiated sheet of neuroepithelial cells, whose differentiation requires the generation and maintenance of the correct cellular polarity. To examine the role of cell polarity in retinal development, we cloned three zebrafish lin7 genes (lin7a, lin7b, and lin7c), which each encodes a protein candidate that is required for generation/maintenance of neuroepithelial cell junctions. These three zebrafish Lin7 proteins share over 78% amino acid identity and contain both L27 and PDZ domains that are present in all Lin7 homologs. Immunoblots revealed that the Lin7b and Lin7c proteins were first expressed in the developing eye by 24hr postfertilization (hpf), while Lin7a was not detected in the eye until 72 hpf. At 33 hpf, the Lin7 proteins localized at, or slightly apical of, the actin-associated adherens junctions in the retinal neuroepithelium. This subcellular distribution required the expression of the Nok protein. In the absence of Nok, the Lin7 proteins failed to localize to either the ectopic adherens junctions or the cell membrane. At 4 days postfertilization, in situ hybridisation revealed that all three lin7 genes were expressed in both the ganglion cell layer and the bipolar cell region of the inner nuclear layer. The lin7a gene was also expressed in the amacrine and horizontal cell regions of the inner nuclear layer, while lin7c was also expressed in the outer nuclear layer. In the adult retina, where Lin7a is the predominant form expressed, the Lin7 proteins were localized to the outer and inner plexiform layers, the bipolar and horizontal cells of the inner nuclear layer, and the ganglion cells. These results suggest that the three zebrafish Lin7 proteins possess partially redundant, yet essential, roles in retinal development.

Animals↗
PubMed1995

Development of retinal vasculature is mediated by hypoxia-induced vascular endothelial growth factor (VEGF) expression by neuroglia.

We have studied the role of the hypoxia-inducible angiogenic growth factor vascular endothelial growth factor (VEGF) in the induction and control of vessel growth in the developing retina of rats and cats, using in situ hybridization techniques. VEGF is expressed successively in two layers of neural retina, the innermost (axon) layer and the inner nuclear layer (INL). In the axon layer, VEGF is expressed transiently by astrocytes as they spread across the layer, closely preceding the formation of superficial vessels. In the INL, VEGF is expressed transiently by somas at the middle of the layer (presumably Müller cells), closely preceding the formation of the deep layer of retinal vessels. We propose that hypoxia caused by the onset of neuronal activity is detected by strategically located populations of neuroglia, first astrocytes, then Müller cells. In response they secrete VEGF, inducing formation of the superficial and deep layers of retinal vessels, respectively. As the vessels become patent, they relieve the hypoxic stimulus, so vessel formation is matched to oxygen demand. This hypothesis was tested experimentally in three ways. Expression of the high affinity flk-1 receptor for VEGF was demonstrated in newly formed retinal vessels, confirming that the secreted VEGF acts on the vessels, in a paracrine fashion. Direct hypoxic regulation of VEGF expression by macroglia was demonstrated in primary cultures of astrocytes and in cells of a glioma line. Hypoxic regulation of VEGF expression in the intact developing retina was demonstrated by showing that oxygen-enriched atmospheres that inhibit vessel formation also suppress endogenous VEGF production.

Animals↗
PubMed2006

The initial fetal human retinal vasculature develops by vasculogenesis.

There is increasing evidence that the hemangioblast, a common progenitor for hematopoietic cells and endothelial cells, participates in embryonic and extra-embryonic vasculogenesis in some organs. Whether resident angioblasts or endothelial progenitor cells (EPCs) contribute to human retinal vasculogenesis is still a matter of controversy. To address this controversy, fetal human retinas of 6-23 weeks gestation (WG) were examined using immunohistochemistry and a panel of antibodies against endothelial cell markers (CD34, CD31), a marker for retinal angioblasts and endothelium (CD39/ecto-ADPase), and a marker for precursors and hemangioblasts (CXCR4). Confocal microscopic spectral analysis and double labeling with Ki67 was used to identify the proliferating cell types. In the inner neuroblastic layer of the 6-8 WG retina and in the putative ganglion cell layer in avascular regions of older eyes (14 WG-20 WG), scattered CD39+ angioblasts were well in advance of forming vasculature. There was a layer of CXCR4+ cells in the inner retina that was reduced in size with development. As blood vessels formed, CD39+ cells were always well in advance of the vascular front and they expressed CXCR4. This demonstrates that a pool of resident angioblasts express CD39 and CXCR4 as they differentiate and participate in vasculogenesis in the fetal human. They retain expression of CD39 as endothelial cells in the newly formed retinal vasculature but they down-regulate CXCR4 expression.

Antigens, CD↗
PubMed2005

Human retinal progenitor cells grown as neurospheres demonstrate time-dependent changes in neuronal and glial cell fate potential.

The spatiotemporal birth order of the seven major classes of retinal cells is highly conserved among vertebrates. During retinal development, long projection neurons (ganglion cells) are produced first from resident progenitors, followed by the appearance of retinal interneurons, photoreceptors, and Muller glia. This sequence is maintained through the complex orchestration of cell-intrinsic and cell-extrinsic events and factors, including local influences between neighboring cells. Here we asked whether cultures of human prenatal retinal cells might also yield different ratios of cell types based on gestational age and time spent in vitro, thus recapitulating in vivo development. An established chopping technique was used to passage human prenatal retinal cells as neurospheres, avoiding the use of proteases and preserving cell-cell contacts and native microenvironments present in vivo. Retinal neurospheres cultured in this manner demonstrated specific patterns of growth over a limited time period, possibly reflecting trends in normal retinal development. Upon differentiation, immunocytochemical analysis revealed that retinal neurospheres produce predominantly glial cells with increasing gestational age and time in culture. Conversely, the percentage of betaIII tubulin-positive neurons declined over time. This provides information for optimizing culture systems aimed at the study of human retinal development and the generation of specific retinal cell types for therapeutic use or drug testing.

Cell Culture Techniques↗
PubMed2003

Expression and regulation of L-cystine transporter, system xc-, in the newly developed rat retinal Müller cell line (TR-MUL).

The purpose of the present study was to elucidate the expression and regulation of the L-cystine transporter, system x(c) (-), in Müller cells. In this study, newly developed conditionally immortalized rat Müller cell lines (TR-MUL) from transgenic rats harboring the temperature-sensitive SV 40 large T-antigen gene were used as an in vitro model. TR-MUL cells express large T-antigen and grow well at 33 degrees C with a doubling time of 30 h, but do not grow at 39 degrees C. TR-MUL cells express typical Müller cell markers such as S-100, glutamine synthetase, and EAAT1/GLAST, whereas EAAT2/GLT-1 and EAAT5 are not detected. TR-MUL cells also exhibit little or no expression of glial fibrillary acidic protein. We found that TR-MUL5 cells exhibited [(14)C]L-cystine uptake activity and expressed xCT and 4F2hc, which involve system x(c) (-). The uptake of [(14)C]L-cystine was significantly inhibited by L-glutamic acid and L-aspartic acid, whereas L-leucine had no effect. Following diethyl maleate (DEM) treatment, the glutathione concentration in TR-MUL5 cells was reduced in the first 24 h, then gradually recovered for more than 24 h. The L-cystine uptake rate and the xCT expression level in TR-MUL5 cells were enhanced by DEM treatment. In contrast, the 4F2hc expression level was unchanged. In conclusion, TR-MUL cells have the properties of Müller cells and exhibit system x(c) (-)-mediated L-cystine uptake activity. The oxidative stress conditions following DEM treatment activate L-cystine transport in TR-MUL cells due to the enhanced transcription of the xCT gene.

Animals↗
PubMed1987

[Ophthalmologic prevention in premature infants].

Forty-four of the 262 pupils at the school for blind and visually handicapped children in Nuremberg, i.e., 17%, suffer from sequelae of retinopathy of prematurity (ROP); this condition is currently top of the list of causes of blindness. The risk factors involved were identified by analyzing 294 histories of premature children born between 1981 und 1984. In the case of 16 children, ophthalmoscopic criteria were taken from the 1984 international classification. The data of the children with ROP, at birth and at the time when ROP developed, were recorded on a prognosis card, in each case between the child's absolute age (abscissa) and birthweight in g (ordinate). In this way it was possible to read off the critical phase of retinal development for each newly examined child. This card facilitates monitoring, the provision of forensic evidence, the timing of ophthalmoscopy during critical phases of retinal development, and may also enable further relationships to be detected.

Birth Weight↗
PubMed1990

The early development of retinal ganglion cells with uncrossed axons in the mouse: retinal position and axonal course.

The carbocyanine dye, DiI, has been used to study the retinal origin of the uncrossed retinofugal component of the mouse and to show the course taken by these fibres through the optic nerve and chiasm during development. Optic axons first arrive at the chiasm at embryonic day 13 (E13) but do not cross the midline until E14. After this stage, fibres taking an uncrossed course can be selectively labelled by unilateral tract implants of DiI. The earliest ipsilaterally projecting ganglion cells are located in the dorsal central retina. The first sign of the adult pattern of distribution of ganglion cells with uncrossed axons located mainly in the ventrotemporal retina is seen on embryonic day 16.5, thus showing that the adult line of decussation forms early in development. A small number of labelled cells continue to be found in nasal and dorsal retina at all later stages. At early stages (E14-15), retrogradely labelled uncrossed fibres are found in virtually all fascicles of the developing nerve, intermingling with crossed axons throughout the length of the nerve. At later stages of development (E16-17), although uncrossed fibres pass predominantly within the temporal part of the stalk, they remain intermingled with crossed axons. A significant number of uncrossed axons also lie within the nasal part of the optic stalk. The position of uncrossed fibres throughout the nerve in the later developmental stages is comparable to that seen in the adult rodent (Baker and Jeffery, 1989). The distribution of uncrossed axons thus indicates that positional cues are not sufficient to account for the choice made by axons when they reach the optic chiasm.

Animals↗