Home About us Contact
|
Home About us Contact | ||
|
|
||
Inner Retina (inner + retina)
Selected AbstractsSynaptic plasticity and functionality at the cone terminal of the developing zebrafish retinaDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2003Oliver Biehlmaier Abstract Previous studies have analyzed photoreceptor development, some inner retina cell types, and specific neurotransmitters in the zebrafish retina. However, only minor attention has been paid to the morphology of the synaptic connection between photoreceptors and second order neurons even though it represents the transition from the light sensitive receptor to the neuronal network of the visual system. Here, we describe the appearance and differentiation of pre- and postsynaptic elements at cone synapses in the developing zebrafish retina together with the maturation of the directly connecting second order neurons and a dopaminergic third order feedback-neuron from the inner retina. Zebrafish larvae were examined at developmental stages from 2 to 7dpf (days postfertilization) and in the adult. Synaptic maturation at the photoreceptor terminals was examined with antibodies against synapse associated proteins. The appearance of synaptic plasticity at the so-called spinule-type synapses between cones and horizontal cells was assessed by electron microscopy, and the maturation of photoreceptor downstream connection was identified by immunocytochemistry for GluR4 (AMPA-type glutamate receptor subunit), protein kinase ,1 (mixed rod-cone bipolar cells), and tyrosine hydroxylase (dopaminergic interplexiform cells). We found that developing zebrafish retinas possess first synaptic structures at the cone terminal as early as 3.5dpf. Morphological maturation of these synapses at 3.5,4dpf, together with the presence of synapse associated proteins at 2.5dpf and the maturation of second order neurons by 5dpf, indicate functional synaptic connectivity and plasticity between the cones and their second order neurons already at 5dpf. However, the mere number of spinules and ribbons at 7dpf still remains below the adult values, indicating that synaptic functionality of the zebrafish retina is not entirely completed at this stage of development. © 2003 Wiley Periodicals, Inc. J Neurobiol 56: 222,236, 2003 [source] Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptorsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004Afrim H. Bytyqi Abstract Blinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE,/, retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss-cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild-type, but in the AChE,/, mouse their processes become structured within two ,novel' sublaminae. During this early period, photoreceptors become arranged regularly and at a normal rate in the AChE,/, retina. However, during the following 75 days, first their outer segments, and then the entire photoreceptor layer completely degenerate by apoptosis. Eventually, cells of the inner retina also undergo apoptosis. As butyrylcholinesterase (BChE) is present at a normal level in the AChE,/, mouse, the observed effects must be solely due to the missing AChE. These are the first in vivo findings to show a decisive role for AChE in the formation of the inner retinal network, which, when absent, ultimately results in photoreceptor degeneration. [source] Morphological characterization of retinal bipolar cells in the marine teleost Rhinecanthus aculeatusTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 15 2010Vincenzo Pignatelli Abstract The marine teleost Rhinecanthus aculeatus (Balistidae) has recently been shown to posses trichromatic color vision supported by a retinal combination of double and single cones. Double cones are composed of two members with different spectral sensitivity. It is not known whether a correlation exists between the chromatic wiring of double cones to the inner retina and trichromacy, nor how unmixed, chromatic information is extracted from the two members of the couple. In mammalians, bipolar cells determine color segregation by means of the midget system, central to trichromatic color vision; however, midget bipolar cells have never been described in teleosts. On the basis of its likely importance in transferring chromatic photoreceptor signals to the inner retina, we have morphologically characterized the retinal bipolar cell types of R. aculeatus using DiOlistic staining techniques to verify if an anatomical specialization of this group of cells is required to support trichromatic color vision. Thirteen cell types are described: eight putative OFF types and five putative ON types. Of these, four had axonal boutons ramifying in both sublayers (ON and OFF) of the inner plexiform layer, six had terminals restricted to the OFF layer, and three cell types had terminals restricted to the ON layer. Dendritic arbors of bipolar cells had narrower diameters (5,40 ,m) in comparison to bipolar cells of other teleost species; this supports the idea that a low degree of photoreceptor to bipolar convergence is correlated with trichromacy in this retina and possibly with the function of double cones as color receptors. J. Comp. Neurol. 518:3117,3129, 2010. © 2010 Wiley-Liss, Inc. [source] Retinal organization in the retinal degeneration 10 (rd10) mutant mouse: A morphological and ERG studyTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2007Claudia Gargini Abstract Retinal degeneration 10 (rd10) mice are a model of autosomal recessive retinitis pigmentosa (RP), identified by Chang et al. in 2002 (Vision Res. 42:517,525). These mice carry a spontaneous mutation of the rod-phosphodiesterase (PDE) gene, leading to a rod degeneration that starts around P18. Later, cones are also lost. Because photoreceptor degeneration does not overlap with retinal development, and light responses can be recorded for about a month after birth, rd10 mice mimic typical human RP more closely than the well-known rd1 mutants. The aim of this study is to provide a comprehensive analysis of the morphology and function of the rd10 mouse retina during the period of maximum photoreceptor degeneration, thus contributing useful data for exploiting this novel model to study RP. We analyzed the morphology and survival of retinal cells in rd10 mice of various ages with quantitative immunocytochemistry and confocal microscopy; we also studied retinal function with the electroretinogram (ERG), recorded between P18 and P30. We found that photoreceptor death (peaking around P25) is accompanied and followed by dendritic retraction in bipolar and horizontal cells, which eventually undergo secondary degeneration. ERG reveals alterations in the physiology of the inner retina as early as P18 (before any obvious morphological change of inner neurons) and yet consistently with a reduced band amplification by bipolar cells. Thus, changes in the rd10 retina are very similar to what was previously found in rd1 mutants. However, an overall slower decay of retinal structure and function predicts that rd10 mice might become excellent models for rescue approaches. J. Comp. Neurol. 500:222,238, 2007. © 2006 Wiley-Liss, Inc. [source] Cellular patterns in the inner retina of adult zebrafish: Quantitative analyses and a computational model of their formationTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2004David A. Cameron Abstract The mechanisms that control cellular pattern formation in the growing vertebrate central nervous system are poorly understood. In an effort to reveal mechanistic rules of cellular pattern formation in the central nervous system, quantitative spatial analysis and computational modeling techniques were applied to cellular patterns in the inner retina of the adult zebrafish. All the analyzed cell types were arrayed in nonrandom patterns tending toward regularity; specifically, they were locally anticlustered. Over relatively large spatial scales, only one cell type exhibited consistent evidence for pattern regularity, suggesting that cellular pattern formation in the inner retina is dominated by local anticlustering mechanisms. Cross-correlation analyses revealed independence between the patterns of different cell types, suggesting that cellular pattern formation may involve multiple, independent, homotypic anticlustering mechanisms. A computational model of cellular pattern formation in the growing zebrafish retina was developed, which featured an inhibitory, homotypic signaling mechanism, arising from differentiated cells, that controlled the spatial profile of cell fate decisions. By adjusting the spatial profile of this decaying-exponential signal, the model provided good estimates of all the cellular patterns that were observed in vivo, as objectively judged by quantitative spatial pattern analyses. The results support the hypothesis that cellular pattern formation in the inner retina of zebrafish is dominated by a set of anticlustering mechanisms that may control events at, or near, the spatiotemporal point of cell fate decision. J. Comp. Neurol. 471:11,25, 2004. © 2004 Wiley-Liss, Inc. [source] Contribution of voltage-gated sodium channels to the b-wave of the mammalian flash electroretinogramTHE JOURNAL OF PHYSIOLOGY, Issue 10 2008Deb Kumar Mojumder Voltage-gated sodium channels (Nav channels) in retinal neurons are known to contribute to the mammalian flash electroretinogram (ERG) via activity of third-order retinal neurons, i.e. amacrine and ganglion cells. This study investigated the effects of tetrodotoxin (TTX) blockade of Nav channels on the b-wave, an ERG wave that originates mainly from activity of second-order retinal neurons. ERGs were recorded from anaesthetized Brown Norway rats in response to brief full-field flashes presented over a range of stimulus energies, under dark-adapted conditions and in the presence of steady mesopic and photopic backgrounds. Recordings were made before and after intravitreal injection of TTX (,3 ,m) alone, 3,6 weeks after optic nerve transection (ONTx) to induce ganglion cell degeneration, or in combination with an ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 200 ,m) to block light-evoked activity of inner retinal, horizontal and OFF bipolar cells, or with the glutamate agonist N -methyl- d -aspartate (NMDA, 100,200 ,m) to reduce light-evoked inner retinal activity. TTX reduced ERG amplitudes measured at fixed times corresponding to b-wave time to peak. Effects of TTX were seen under all background conditions, but were greatest for mesopic backgrounds. In dark-adapted retina, b-wave amplitudes were reduced only when very low stimulus energies affecting the inner retina, or very high stimulus energies were used. Loss of ganglion cells following ONTx did not affect b-wave amplitudes, and injection of TTX in eyes with ONTx reduced b-wave amplitudes by the same amount for each background condition as occurred when ganglion cells were intact, thereby eliminating a ganglion cell role in the TTX effects. Isolation of cone-driven responses by presenting test flashes after cessation of a rod-saturating conditioning flash indicated that the TTX effects were primarily on cone circuits contributing to the mixed rod,cone ERG. NMDA significantly reduced only the additional effects of TTX on the mixed rod,cone ERG observed under mesopic conditions, implicating inner retinal involvement in those effects. After pharmacological blockade with CNQX, TTX still reduced b-wave amplitudes in cone-isolated ERGs indicating Nav channels in ON cone bipolar cells themselves augment b-wave amplitude and sensitivity. This augmentation was largest under dark-adapted conditions, and decreased with increasing background illumination, indicating effects of background illumination on Nav channel function. These findings indicate that activation of Nav channels in ON cone bipolar cells affects the b-wave of the rat ERG and must be considered when analysing results of ERG studies of retinal function. [source] Retinal and Optic Nerve DiseasesARTIFICIAL ORGANS, Issue 11 2003Eyal Margalit Abstract:, A variety of disease processes can affect the retina and/or the optic nerve, including vascular or ischemic disease, inflammatory or infectious disease, and degenerative disease. These disease processes may selectively damage certain parts of the retina or optic nerve, and the specific areas that are damaged may have implications for the design of potential therapeutic visual prosthetic devices. Outer retinal diseases include age-related macular degeneration, pathologic myopia, and retinitis pigmentosa. Although the retinal photoreceptors may be lost, the inner retina is relatively well-preserved in these diseases and may be a target for retinal prosthetic devices. Inner retinal diseases include retinal vascular diseases such as diabetic retinopathy, retinal venous occlusive disease, and retinopathy of prematurity. Other retinal diseases such as ocular infections (retinitis, endophthalmitis) may affect all retinal layers. Because the inner retinal cells, including the retinal ganglion cells, may be destroyed in these diseases (inner retinal or whole retinal), prosthetic devices that stimulate the inner retina may not be effective. Common optic nerve diseases include glaucoma, optic neuritis, and ischemic optic neuropathy. Because the ganglion cell nerve fibers themselves are damaged, visual prosthetics for these diseases will need to target more distal portions of the visual pathway, such as the visual cortex. Clearly, a sound understanding of retinal and optic nerve disease pathophysiology is critical for designing and choosing the optimal visual prosthetic device. [source] 3122: Regulation of retinal tissue oxygenationACTA OPHTHALMOLOGICA, Issue 2010CJ POURNARAS Purpose To evaluate the changes in the retinal oxygen partial pressure (PO2) following physiological stimuli. Methods Evaluation of either the preretinal and intraretina partial pressure of oxygen (PO2) distribution, using oxygen sensitive microelectrodes, in various animal models. Measurements were obtained during changes of the perfusion pressure, systemic hyperoxia, hypoxia, hypercapnia, carbogen breathing and following carbonic anydrase inhibitors use. Results The oxygen tension (PO2) in the inner half of the retina remains largely unaffected by moderate changes in perfusion pressure. The increase of the systemic PaO2 through breathing of 100% O2 (hyperoxia) induces endothelin (ET) mediated marked vasoconstriction of the inner retinal arterioles in both anesthetized animals and normal human subjects. The regulatory vasoconstriction maintains the PO2 in retinal tissue constant. A decrease in PaO2 (hypoxia) induces a vasodilation of the retinal arterioles through endothelium-derived NO release. As a result, trans-retinal PO2 profiles made during steps of systemic hypoxia have shown that the values measured in the inner retina up to half of its thickness, remain rather stable. By contrast, the PO2 values, measured close to the choroid and in the outer retina, decrease in a linear manner with the decrease of the PaO2. An increase in the PaCO2 (hypercapnia) of arteriolar blood, produces an increase in retinal blood flow and retinal tissue PO2. Intravenous injection of acetazolamide (carbonic anhydrase inhibitor) produces an increase in preretinal PO2 due to dilation of the retinal vessels Conclusion Thanks to the autoregulatory capability of the retinal circulation, the oxygen tension (PO2) in the inner half of the retina, remains largely unaffected during physiological stimuli. [source] 2112: AO imaging of acute macular diseasesACTA OPHTHALMOLOGICA, Issue 2010M PAQUES Purpose To show clinical cases of acute macular diseases and their follow-up by adaptive optics flood imaging. Methods Cases of acute retinal ischemia, of acute macular neuroretinopathy, of photic injury and of poppers-related retinopathy have been observed by a prototypic adaptive optics flood imaging (ImagineEye corporation). Images from follow-up examinations have been registered in order to obtain retinal monitoring at the single photoreceptor level. Iamges were compared to high resolution OCT scans. Results Precise extension and progression/regression of lesions could be documented in all cases. Acute macular neuroretinopathy showed residual cones persisting within an area devoid of any detectable cone. Minute progression and regression of lesions could be documented. Acute ischemia of the inner retina due to central retinal vein occlusion resulted in focal masking of the cone mosaic. The cone mosaic reappeared during follow-up. Photic injury showed no changes over a 1 year follow-up. Images of poppers-related retinopathy showed partial improvement over time. Conclusion Adaptive optics flood imaging allows documentation of the extension and progression of acute maculopathies of various origins. [source] 2412: Laser and oxygenACTA OPHTHALMOLOGICA, Issue 2010CJ POURNARAS Purpose To evaluate the changes in the retinal oxygen partial pressure (PO2) following photocoagulation as well as the resulting effect of the laser induced improved oxygenation, on the retinal vessels hemodynamics. Methods Measurements of the partial pressure of oxygen (PO2) distribution within the retina in various animal species using oxygen sensitive microelectrodes and evaluation of changes on the retinal vessels reactivity, following laser treatment, gave additional insights concerning photocoagulation mechanisms. Results Preretinal intervascular PO2 , far away from vessels, remain constant in all retinal areas. Intervascular intraretinal PO2 gradually decreases from both the vitreo-retinal interface and the choroid towards the mid-retina. Close to the pigment epithelium, it is significantly higher than at the vitreoretinal interface due to the much higher O2 supply provided by choroidal compaires to retinal circulation. Laser photocoagulation reduces the outer retina O2 consumption and allows O2 diffusion into the inner retina from the choroid raising the PO2 in the inner healthy retinal layers and in the preretinal intervascular normal areas. In this way, laser treatment relieves retinal hypoxia in experimental branch vein occlusion (BRVO). In patients with diabetic retinopathy (DR), the retinal PO2 is also higher in areas previously treated with laser. Following photocoagulation, the resulting reversal of hypoxia, the down-regulation of the VEGF expression, the retinal vasculature constriction and the improvement of the auto-regulatory response to physiological stimuli, all affect favorably both the retinal neovascularisation and macular edema. Conclusion Photocoagulation induces an increase of the inner retinal oxygenation resulting to an improvement of the autoregulatory retinal vessels response. [source] Retinal photocoagulation and oxygenationACTA OPHTHALMOLOGICA, Issue 2009CJ POURNARAS Purpose The clinical role of photocoagulation for the treatment of hypoxia related complications of retinal ischemic microangiopathies is well established. Methods Measurements of the partial pressure of oxygen (PO2) distribution within the the retina in various animal species using oxygen sensitive microelectrodes and evaluation of the retinal vessels reactivity by laser doppler velocimetry gave additional insights concerning photocoagulation mechanisms. Results The PO2 within the vitreo-retinal interface is heterogeneous. Preretinal and trans-retinal PO2 profiles indicate that the preretinal PO2 far away from vessels remain constant in all retinal areas. Intervascular intraretinal PO2 gradually decreases from both the vitreo-retinal interface and the choroid towards the mid-retina. Close to the pigment epithelium, it is significantly higher than at the vitreoretinal interface due to the much higher O2 supply provided by choroidal compaires to retinal circulation. Laser photocoagulation reduces the outer retina O2 consumption and allows O2 diffusion into the inner retina from the choroid raising the PO2 in the inner healthy retinal layers and in the preretinal intervascular normal areas. In this way laser treatment relieves retinal hypoxia in experimental branch vein occlusion (BRVO). In patients with diabetic retinopathy (DR), the retinal PO2 is higher in areas previously treated with laser. Following photocoagulation, the resulting reversal of hypoxia, the retinal vasculature constriction and the improvement of the regulatory response to hyperoxia all affect favorably both the retinal neovascularisation and macular edema. Conclusion Photocoagulation induces an increase of the inner retinal oxygenation reversing the retinal hypoxia and improving the regulatory response of the retinal vessels [source] Retinal vessel oximetry using sequential and 'snapshot' hyperspectral imagingACTA OPHTHALMOLOGICA, Issue 2009A MCNAUGHT Purpose Use of sequential, and 'snapshot' hyperspectral imagers to measure oxygen saturation in retinal vessels in normals, and examples of eye disease, eg glaucoma, and retinovascular diseases. Validation of estimated oximetry values using a model eye. Methods A sequential hyperspectral imager was constructed using a fundus camera with built-in liquid-crystal tuneable filter. Images of normals,and ocular disease are presented. A novel 'snapshot' hyperspectral imager is also described: this produces images in a single exposure. Validation of both devices using an artificial eye with capillary tubes containing human blood of known oxygen saturation, placed in front of an 'artificial retina' is described. The image analysis used to detect retinal vessels, and generate oximetric values is detailed. Results Both the sequential, and 'snapshot' retinal imagers produced accurate estimations of retinal vessel oxygen saturation, when compared with the model eye. Imaging of a small group of glaucoma eyes showed abnormally elevated venous oxygen saturation. In proliferative diabetic retinopathy, abnormally elevated venular saturation was found in areas of capillary loss on FFA. In vein occlusion, elevated venous saturation was found in eyes with ischaemic FFAs. Conclusion Both the sequential and 'snapshot' hyperspectral imagers deliver useful oximetric maps of the retina. The 'snapshot' device allows more rapid imaging. The elevated venular oxygen saturation seen in both glaucoma, and retinovascular disease, is perhaps evidence of reduced oxygen consumption in damaged inner retina in glaucoma, and/or vascular 'shunting' in retinovascular disease. [source] The therapeutic effects of retinal laser treatment and vitrectomy.ACTA OPHTHALMOLOGICA, Issue 5 2001A theory based on oxygen, vascular physiology ABSTRACT. The physiologic mechanism of photocoagulation can been seen in the following steps. The physical light energy is absorbed in the melanin of the retinal pigment epithelium. The adjacent photoreceptors are destroyed and are replaced by a glial scar and the oxygen consumption of the outer retina is reduced. Oxygen that normally diffuses from the choriocapillaris into the retina can now diffuse through the laser scars in the photoreceptor layer without being consumed in the mitochondria of the photoreceptors. This oxygen flux reaches the inner retina to relieve inner retinal hypoxia and raise the oxygen tension. As a result, the retinal arteries constrict and the bloodflow decreases. Hypoxia relief reduces production of growth factors such as VEGF and neovascularization is reduced or stopped. Vasoconstriction increases arteriolar resistance, decreases hydrostatic pressure in capillaries and venules and reduces edema formation according to Starling's law. Vitrectomy also improves retinal oxygenation by allowing oxygen and other nutrients to be transported in water currents in the vitreous cavity from well oxygenated to ischemic areas of the retina. Vitrectomy and retinal photocoagulation both improve retinal oxygenation and both reduce diabetic macular edema and retinal neovascularization. [source] | |||||||||||||