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At least 1,693 records · Page 94Linked to original sources
PubMed1978

Genetic control of retinal ganglion cell projections.

We have assessed the effects of 15 pigmentation mutations on the development of retinal ganglion cell projections in mice in two ways: (1) by analyzing the pattern of innervation of the ipsilateral lateral geniculate nucleus as mapped in autoradiograms of brains of animals killed 12 days after intravitreal injection of 3H-proline into one eye and (2) by determining the ratio of axonally transported radioactive protein in the contralateral and ipsilateral optic tracts after similar intravitreal injections. Analysis of the ratio of transported protein in the two optic tracts provides a new and useful assay of the degree of decussation in experimental animals. The effects of the mutations on eye pigmentation, whole eye melanin content and relative tyrosinase activity also were examined. The degree of ipsilateral innervation generally correlates with the degree of pigmentation of the retinal pigment epithelium and with tyrosinase activity. However, discrepancies have been found in ch and ce mutants. In these animals the pigment epithelium is well pigmented, and the area of ipsilateral innervation in the lateral geniculate nucleus is extensive, despite a high ratio of label in contralateral to ipsilateral optic tracts and low tyrosinase activity. Furthermore, mice heterozygous for the c2J allele have pigmentation and optic projections that are normal even though tyrosinase is reduced to 40% of normal. The few anomalous results suggest that alternative or additional factors may control optic axon projections.

Alleles↗
PubMed1998

Retrovirus-mediated gene transfer targeted to retinal photocoagulation sites.

Diabetic retinopathy is a major cause of acquired blindness due to the development of retinal neovascularization and associated traction retinal detachment. It is commonly treated with retinal photocoagulation therapy; however, progression to blindness remains a significant problem. To determine the feasibility of adjunctive anti-angiogenic gene therapy, we evaluated the capability of retroviral vectors, which transfer exogenous genes only into dividing cells, to transfer and express a beta-galactosidase gene selectively into photocoagulation sites. Thirty-five rabbits received 30 retinal photocoagulation burns in the right eye followed 2 days later by beta-galactosidase (G1nBgSvNa) or control (G1XSvNa) vector injection into the subretinal space. Beta-galactosidase expression was observed in the photocoagulation sites from 5 days after vector administration (31.7+/-7.0%) to 12 weeks (6.7+/-3.4%). Immunohistochemical studies of the treated retinas using antibody Ber-MAC3 and anti-cytokeratin antibodies revealed that transduced cells were macrophages and retinal pigment epithelial cells. To determine feasibility in a primate, two monkeys received 10 laser burns in the macula superior to the fovea followed 2 days later by G1nBgSvNa vector. beta-galactosidase expression was found in photocoagulation sites and foveal retina was well preserved. We conclude that gene transfer to retinal photocoagulation sites provides stable expression of the transduced gene with relatively high efficiency. This feasibility study suggests the possibility of transferring genes encoding for anti-angiogenic factors into photocoagulation sites to improve the efficacy of laser photocoagulation therapy.

Angiography↗
PubMed1988

Foscarnet as treatment for cytomegalovirus retinitis following bone marrow transplantation.

This report describes a patient with chronic granulocytic leukaemia who developed cataracts on busulphan treatment. Following allogeneic bone marrow transplantation, he developed cytomegalovirus retinitis, which was treated successfully with trisodium phosphonoformate (foscarnet). Cytomegalovirus retinitis and its therapy, and busulphan-induced cataract are discussed.

Adult↗
PubMed2006

Specificity of cone inputs to macaque retinal ganglion cells.

The specificity of cone inputs to ganglion cells has implications for the development of retinal connections and the nature of information transmitted to higher areas of the brain. We introduce a rapid and precise method for measuring signs and magnitudes of cone inputs to visual neurons. Colors of stimuli are modulated around circumferences of three color planes in clockwise and counterclockwise directions. For each neuron, the projection of the preferred vector in each plane was estimated by averaging the response phases to clockwise and counterclockwise modulation. The signs and weights of cone inputs were derived directly from the preferred vectors. The efficiency of the method enables us to measure cone inputs at different temporal frequencies and short-wavelength-sensitive (S) cone adaptation levels. The results show that S-cone inputs to the parvocellular and magnocellular ganglion cells are negligible, which implies underlying connectional specificity in the retinal circuitry.

Action Potentials↗
PubMed1998

Advanced glycation end products increase retinal vascular endothelial growth factor expression.

Advanced glycation end products (AGEs) are linked with the development of diabetic retinopathy; however, the pathogenic mechanisms are poorly defined. Vascular endothelial growth factor (VEGF) levels are increased in ischemic and nonischemic diabetic retina, and VEGF is required for the development of retinal and iris neovascularization. Moreover, VEGF alone can induce much of the concomitant pathology of diabetic retinopathy. In this study, we found that AGEs increased VEGF mRNA levels in the ganglion, inner nuclear, and retinal pigment epithelial (RPE) cell layers of the rat retina. In vitro, AGEs increased VEGF mRNA and secreted protein in human RPE and bovine vascular smooth muscle cells. The AGE-induced increases in VEGF expression were dose- and time-dependent, inhibited by antioxidants, and additive with hypoxia. Use of an anti-VEGF antibody blocked the capillary endothelial cell proliferation induced by the conditioned media of AGE-treated cells. AGEs may participate in the pathogenesis of diabetic retinopathy through their ability to increase retinal VEGF gene expression.

Animals↗
PubMed2001

Colocalization of neuropilin-1 and Flk-1 in retinal neovascularization in a mouse model of retinopathy.

PURPOSE: To investigate the mechanisms of the development of retinal neovascularization, the localizations of vascular endothelial (VEGF) receptors Flk-1 and neuropilin (NP)-1 mRNAs were examined. METHODS: The model of retinopathy of prematurity (ROP) was produced by ischemia-induced ocular neovascularization, by exposing postnatal day-7 mice to 75% oxygen for 5 days and then returning them to room air for 5 days. Retinal neovascularization was visualized by injection of fluorescein-dextran. Expression of Flk-1 and NP-1 mRNAs were examined by in situ hybridization with flatmount and serial sections of the retina. The localization of NP-1 was also confirmed by immunohistochemistry. Blood vessel patterns were characterized by immunohistochemical localization of von Willebrand factor (vWF). RESULTS: Flatmount in situ hybridization showed intense expression of NP-1 and Flk-1 mRNAs colocalized in the area of neovascularization. In situ hybridization of serial sections of the retina revealed that expression of Flk-1 and NP-1 was restricted to neovascularized vessels of the retina from ROP mice. CONCLUSIONS: The restricted expression of Flk-1 and NP-1 on neovascularized vessels suggests that these molecules may play important roles in retinal neovascularization. This is the first report of the colocalization of NP-1 and Flk-1 on neovascularized vessels of the retina from ROP mice.

Animals↗
PubMed1995

Neurotransmitter receptors of starburst amacrine cells in rabbit retinal slices.

The receptor pharmacology of cholinergic ("starburst") amacrine cells was studied in a newly developed rabbit retinal slice preparation with whole-cell patch clamp. Displaced starburst cells were labeled with the fluorescent dye 4,6-diamidino-2-phenylindole (DAPI), and their dendritic morphology was identified in the slice with Lucifer yellow. Under conditions in which synaptic transmission was blocked by Cd2+, starburst cells responded vigorously to the bath-applied neurotransmitters GABA, glycine, and glutamate. The response to GABA consisted of an inward current and an increase in noise, which could be mimicked by the GABAA agonists muscimol and trans-4-aminocrotonic acid (TACA), but not by the GABAB agonist baclofen or the GABAC agonist cis-4-aminocrotonic acid (CACA). The GABA-evoked currents were reversibly inhibited by bicuculline and picrotoxin and had a reversal potential close to the chloride equilibrium potential. Noise analysis of GABA-activated whole-cell currents yielded elementary conductance estimates of 12.5 pS. Glycine (30-200 microM) also activated a Cl- conductance in starburst cells, which could be completely blocked by strychnine. The non-NMDA agonists kainate (KA, 30-100 microM) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 60 microM) evoked robust responses, which were reversibly blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and which reversed near the equilibrium potential for cations. NMDA coapplied with glycine in salines free of Cd2+ and Mg2+ elicited small but detectable responses. The I/V relation of the NMDA-evoked response showed a characteristic "J"-shaped region in a saline containing 1 mM Mg2+ and 0 Cd2+, indicating that NMDA receptors were present directly on starburst cells. This was consistent with our finding that whole-cell currents evoked by KA and NMDA had different noise characteristics. These results place new constraints on models of starburst cell function and suggest that GABA-mediated inhibition of the starburst cell itself may play an important role in directional selectivity in the retina.

Animals↗
PubMed2003

Adenylate cyclase 1 as a key actor in the refinement of retinal projection maps.

cAMP occupies a strategic position to control neuronal responses to a large variety of developmental cues. We have analyzed the role of calcium-stimulated adenylate cyclase 1 (AC1) in the development of retinal topographic maps. AC1 is expressed in retinal ganglion cells (RGCs) from embryonic day 15 to adulthood with a peak during the first postnatal week. At that time, the other calcium-stimulated AC, AC8, is expressed in the superior colliculus (SC) but not in the RGCs. In mice of the barrelless strain, which carry an inactivating mutation of the AC1 gene, calcium-stimulated AC activity is reduced by 40-60% in the SC and retina. RGC projection maps were analyzed with a variety of anterograde and retrograde tracers. After an initially normal development until postnatal day 3, retinal fibers from the ipsilateral and contralateral eye fail to segregate into eye-specific domains in the lateral geniculate nucleus and the SC. Topographic defects in the fine tuning of the retinotectal and retinogeniculate maps are also observed with abnormalities in the confinement of the retinal axon arbors in the anteroposterior and mediolateral dimensions. This is attributable to the lack of elimination of misplaced axon collaterals and to the maintenance of a transient ipsilateral projection. These results establish an essential role of AC1 in the fine patterning of the retinal map. Calcium-modulated cAMP production in the RGCs could constitute an important link between activity-dependent changes and the anatomical restructuring of the retinal terminal arbors within central targets.

Adenylyl Cyclases↗
PubMed1997

Pathogenic mechanisms in proliferative vitreoretinopathy.

Landmarks in the development of treatment of retinal detachment include the recognition of the significance of retinal breaks that resulted in the distinction between rhegmatogenous retinal detachment (RRD) and exudative retinal detachment, the development of indirect ophthalmoscopy and scleral depression that allow better visualization of the peripheral area of the retina and better identification of retinal breaks, the recognition of the need to seal all retinal breaks, and the realization that vitreous traction is the major underlying cause of retinal tears and RRD. Scleral buckling procedures combine retinopexy to provide a scar around retinal breaks to seal them and scleral indentation to neutralize vitreous traction; they provided the first effective treatment of RRD. As surgeons gained experience with scleral buckling, they became aware that some RRDs, particularly those with fixed folds and/or a funnel configuration, often could not be repaired using this approach. It was thought that excessive vitreous traction was at fault, and the condition was called "massive vitreous retraction."

Animals↗
PubMed1994

Streptokinase-induced Tenon's hemorrhage after retinal detachment surgery.

PURPOSE/METHODS: We studied a case in which a streptokinase-induced Tenon's hemorrhage developed after retinal detachment surgery. The patient received intravenous streptokinase for myocardial infarction two hours after pars plana vitrectomy and encircling scleral buckling surgery. RESULTS/CONCLUSIONS: A Tenon's hemorrhage with an orbital compartment syndrome developed in the patient's left eye, and he underwent lateral canthotomy and inferior cantholysis. Symptoms of the compartment syndrome resolved and final visual acuity was 20/40. Although there are potential ocular-related side effects to thrombolytic therapy, there has been no permanent ocular morbidity reported after thrombolytic-related hemorrhage. We recommend not to defer such life-saving therapy after ocular surgery.

Eye Hemorrhage↗
PubMed1994

Development of muscarinic acetylcholine receptors in the ferret retina.

The development of muscarinic acetylcholine receptor protein in the ferret retina was studied using biochemical, autoradiographic, and light and electron microscopic immunohistochemical techniques. The development of retinal muscarinic cholinergic receptor proteins involves transient shifts in their number and distribution, as well as changes in the relative abundance of two molecular weight variants. Receptor binding assays demonstrate changes in the number and affinity of retinal binding sites for the muscarinic cholinergic ligand [3H]quinuclidinylbenzilate ([3H]QNB). Light microscopic immunohistochemical studies reveal the presence of muscarinic acetylcholine receptor-like (mAChR-like) immunoreactivity in the adult inner plexiform layer. During development, the mAChR-like immunoreactivity appears in a number of other retinal layers. Electron microscopic immunohistochemical studies indicate that muscarinic acetylcholine receptor-like immunoreactivity is found at amacrine-amacrine cell contacts. Both autoradiographic and gel slice electrophoretic studies were carried out after labeling of developing and adult retinal muscarinic receptors with [3H]propylbenzilylcholine mustard ([3H]propylbenzilylcholine mustard ([3H]PrBCM), which irreversibly labels the muscarinic acetylcholine receptor. Polyacrylamide gel electrophoresis under reducing, denaturing conditions resolved two peaks of radioactivity corresponding to [3H]PrBCM-labeled protein; both were eliminated by pre- and co-incubation of labeled adult retinas with excess atropine. Combined with the results of earlier studies, these observations suggest that the subtypes, number and distribution of muscarinic receptor proteins changes during retinal synaptogenesis.

Aging↗
PubMed1989

Retinal ganglion beta cells project transiently to the superior colliculus during development.

In adult cats, retinal ganglion cells of the beta class project almost exclusively to the lateral geniculate nucleus rather than to the superior colliculus (SC). We have examined whether this target specificity is present during early development. To identify ganglion cells that send axons to the SC in development, rhodamine-labeled microspheres were deposited in the SC at embryonic day (E) 38, E43, or postnatal day (P) 4. Retinae were then removed between E56 and P32 and kept alive in a tissue-slice chamber so that ganglion cells that had been retrogradely labeled with microspheres could be injected intracellularly with Lucifer yellow to reveal their morphological class. Many beta cells could be retrogradely labeled by microspheres injected into the SC at E38 or E43. They were indistinguishable from beta cells projecting to the lateral geniculate nucleus and were found even when a single injection was restricted to the caudal portion of the SC. In contrast, beta cells could not be retrogradely labeled by microspheres injected into the SC at P4. The disappearance of a beta-cell projection to the SC cannot be explained entirely by cell death since as late as P32, well after the major period of ganglion cell death, many beta ganglion cells labeled with microspheres at E38 were still present. These observations suggest that many beta cells initially extend an axon collateral to the SC that is subsequently lost some time after E43. Thus, to achieve the remarkable specificity present in the adult visual system, beta cells must withdraw axon collaterals from an entire target nucleus. Similar collateral elimination may give rise to the specificity of afferent connections in other sensory systems.

Animals↗
PubMedDate not supplied

Neovascular glaucoma associated with cilioretinal artery occlusion combined with perfused central retinal vein occlusion.

BACKGROUND: Cilioretinal artery occlusion rarely results in neovascular glaucoma, especially in cases of extensive cilioretinal infarction and combined retinal vascular occlusion. CASE: A 62-year-old man with diabetes mellitus and essential hypertension showed a visual acuity of counting fingers, retinal whitening temporal to the optic disc with mild dilation and tortuosity of the retinal veins, and retinal hemorrhages in four quadrants of his right eye. Fluorescein angiography demonstrated a delayed filling of the central retinal vein and cilioretinal artery. OBSERVATIONS: Two months later, neovascular glaucoma developed and retinal ablation was performed using an argon laser. Trabeculectomy was also performed due to the intractability of the glaucoma, and central artery occlusion was found. On magnetic resonance angiography, the right distal common carotid artery was irregularly narrowed and the right ophthalmic artery was almost entirely occluded. CONCLUSIONS: In cases of cilioretinal artery occlusion and perfused central retinal vein occlusion with multiple risk factors, close follow-up is advised.

Ciliary Arteries↗
PubMedDate not supplied

[Intraoperative diagnosis of retinal ruptures in rhegmatogenous retinal detachment in avitreous eyes by using a coloring agent].

Sixteen patients were operated for regmatogene retinal detachment developed at different time periods after a previously made vitrectomy; no retinal ruptures were found in preoperative examinations. The method of colouring with subretinal fluid, 0.1% fluorescence solution, was intraoperatively used for the detection of such ruptures. The coloured fluid escaped from the subretinal cavity through a retinal rapture into the vitreal cavity, which ensured an easy visualization of ruptures. Retinal ruptures could be detected in all 16 (100%) patients. They were located in 8 (50%) cases in the zone of previously made sclerotomy and were regarded as an outcome of the local proliferative vitreoretinopathy on the remains of the basic vitreous elements.

Female↗
PubMed1983

Optic nerve sarcoidosis: a report of three cases.

Three cases are reported of sarcoidosis, confirmed by a positive Kveim-Silzbach test, presenting with optic nerve swelling. One case subsequently developed gross peripheral retinal ischaemia. Two cases developed peripapillary disciform lesions, with subretinal neovascularization.

Adult↗
PubMedDate not supplied

Ocular manifestations of AIDS.

1. Cytomegalovirus retinitis is the leading cause of AIDS-related blindness. 2. Patients with reduced CD4 counts are at risk of developing cytomegalovirus retinitis and should be informed of symptoms (floaters, scotoma) and should have periodic dilated retina examinations. 3. AIDS patients who develop herpes zoster should be monitored for progressive outer retinal necrosis.

AIDS-Related Opportunistic Infections↗
PubMed2004

Neurotrophic regulation of retinal ganglion cell synaptic connectivity: from axons and dendrites to synapses.

This review highlights important events during the morphological development of retinal ganglion cells (RGCs), focusing on mechanisms that control axon and dendritic arborization as a means to understand synaptic connectivity with special emphasis on the role of neurotrophins during structural and functional development of RGCs. Neurotrophins and their receptors participate in the development of visual connectivity at multiple levels. In the visual system, neurotrophins have been shown to exert various developmental influences, from guiding the morphological differentiation of neurons to controlling the functional plasticity of visual circuits. This review article examines the role of neurotrophins, and in particular of BDNF, during the morphological development of RGCs, and discusses potential interactions between activity and neurotrophins during development of neuronal connectivity.

Animals↗