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Results for “retinal plasticity”

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At least 55 records · Page 3Linked to original sources
PubMed2004

Competitive interactions between retinal ganglion axons for tectal targets explain plasticity of retinotectal projection in the servomechanism model of retinotectal mapping.

The mechanism of topographic mapping of retinal ganglion cells to the midbrain was previously elucidated by the servomechanism model, which is based on the fact that cells expressing Eph-receptors respond specifically to surface expressing membrane-bound ephrin-ligands at a critical level. The retina has increased nasal-to-temporal gradient of Eph receptor-density, and the optic tectum/superior colliculus has increased rostral-to-caudal gradient of membrane-bound ephrin-ligand. An axon from the retina has an identification tag of a certain level of Eph-receptor density depending on its retinal position, and adheres to the site on the tectum/superior colliculus expressing ephrin-ligands at a critical ligand-density level. The servomechanism model rigidly defines positions of axon terminals on the midbrain. However, optic nerve regeneration experiments combined with halved retina or tectum show a plastic or flexible mapping (expansion, compression and transposition of tectal projections). To reconcile the discrepancy between the rigid model and the plastic behavior, competition between retinal axon terminals for a target site was introduced to the servomechanism. The servomechanism/competition model succeeded in computer simulations of the plastic mapping of retinal axons on the tectum. Recent experiments of upregulated ligand-density on the tectum during nerve regeneration and the role of axonal competition are discussed.

Algorithms↗
PubMed1997

Adaptation of retinal processing to image contrast and spatial scale.

Owing to the limited dynamic range of a neuron's output, neural circuits are faced with a trade-off between encoding the full range of their inputs and resolving gradations among those inputs. For example, the ambient light level varies daily over more than nine orders of magnitude, whereas the firing rate of optic nerve fibres spans less than two. This discrepancy is alleviated by light adaptation: as the mean intensity increases, the retina becomes proportionately less sensitive. However, image statistics other than the mean intensity also vary drastically during routine visual processing. Theory predicts that an efficient visual encoder should adapt its strategy not only to the mean, but to the full shape of the intensity distribution. Here we report that retinal ganglion cells, the output neurons of the retina, adapt to both image contrast-the range of light intensities-and to spatial correlations within the scene, even at constant mean intensity. The adaptation occurs on a scale of seconds, one hundred times more slowly than the immediate light response, and involves 2-5-fold changes in the firing rate. It is mediated within the retinal network: two independent sites of modulation after the photoreceptor cells appear to be involved. Our results demonstrate a remarkable plasticity in retinal processing that may contribute to the contrast adaptation of human vision.

Action Potentials↗
PubMed1977

Dissociation of the vitreo-retinal junction following experimental embolization of retinal circulation.

Spheric plastic beads (7-25 mu in diameter) were injected into the central retinal artery of the owl monkey (Aotus trivirgatus) using a micro-surgical technique. The occlusion of retinal arteriolar branches resulted in posterior vitreous detachment and microcystoid degeneration in inner retinal layers. The dissociation of the vitreoretinal junction showed three different entities: detachment of the vitreous from the basal lamina (inner limiting lamina of the retina), separation of the basal lamina from the retina, and detachment of shreds of glial cells and other degenerated retinal tissue (intraretinal schisis).

Animals↗
PubMed2005

Long-term plasticity mediated by mGluR1 at a retinal reciprocal synapse.

The flow of information across the retina is controlled by reciprocal synapses between bipolar cell terminals and amacrine cells. However, the synaptic delays and properties of plasticity at these synapses are not known. Here we report that glutamate release from goldfish Mb-type bipolar cell terminals can trigger fast (delay of 2-3 ms) and transient GABA(A) IPSCs and a much slower and more sustained GABA(C) feedback. Synaptically released glutamate activated mGluR1 receptors on amacrine cells and, depending on the strength of presynaptic activity, potentiated subsequent feedback. This poststimulus enhancement of GABAergic feedback lasted for up to 10 min. This form of mGluR1-mediated long-term synaptic plasticity may provide retinal reciprocal synapses with adaptive capabilities.

Animals↗
PubMed1981

Saccadic plasticity: parametric adaptive control by retinal feedback.

Saccadic gain (the ratio of saccadic amplitude to target eccentricity) was experimentally altered as normal human observers made refixation saccades to the right, which caused step changes in the horizontal position of the target. Eye movements were monitored by diffuse infrared limbus reflection. We found that decreases in saccadic gain reached 60% of completeness, whereas increases were only 25% complete. This asymmetry in adaptive capacity may reflect the saccadic system's need to avoid overshooting a target. With a single target, adaptation is rapid (time constant = 6 saccades); if training is distributed over six different targets, adaptation is considerably slower (time constant = 57 saccades). Gain changes that result from training with a given target do not transfer strongly to other targets in the same horizontal direction and may not transfer at all to targets in the opposite direction. The gain of saccades to one target may be decreased, and simultaneously the gain of saccades to another target at a different distance in the same direction is increased. These results suggest that each element of a sensory-motor structure underlying saccadic plasticity is associated with a particular retinal or spatial sensory locus and can alter its motor response without much affecting the response of neighboring elements. This is consistent with the finding that distributed training slows adaptation.

Eye Movements↗
PubMed1995

Remodeling processes during neural retinal regeneration in adult urodeles: an immunohistochemical survey.

Dynamic features of neural retina regeneration in the adult newt Pleurodeles waltl were analyzed using immunohistochemical studies. Antibody to Glial Fibrillary Acidic Protein (GFAP) was used as a marker of the retinal glial supportive system in order to obtain an overview of the retinal reorganization pattern. Unexpectedly, retinal progenitor cells displayed GFAP staining, as did later Müller glial processes and astrocytes supporting ganglional axons. To study changes of plasticity during retinal restoration, the expression patterns of highly- (PSA) and weakly-sialylated N-CAM were examined by double staining. In the retina of adult newts, a sustained expression of total-N-CAM and PSA-N-CAM was detected. However, while an intense distribution of N-CAM was observed throughout the retina, PSA labeling was especially seen in the outer retinal layers. During retinal regeneration, similar widespread staining patterns were observed with the two antibodies, but labeling appeared higher with anti-total-N-CAM antibody than with anti-PSA-N-CAM antibody. On the other hand, tenascin (Tn) expression was analyzed for the first time during retinal regeneration. At the early stages, brightly stained matrix fibers of abundant Tn accumulating in the eye cavity were seen close to the retinal rudiment cells, which suggested that Tn was secreted from these cells. Tn expression was seen nearly throughout the retinal regenerate during neurite migration and then became restricted to the plexiform layers. In the light of the functions attributed to N-CAM and Tn in histogenetic events, the putative roles played by these morphoregulatory molecules in adult newt retinal regeneration were discussed.

Animals↗
PubMed1983

Alterations in retinal neurotransmitter receptors and neuropeptides of the chick by kainic acid and acrylamide.

The effects of intraocular injection of kainic acid and acrylamide upon retinal neuropeptides and high affinity binding sites have been determined in the chick. Kainic acid causes a sharp reduction in Met-enkephalin and somatostatin while neurotensin levels are unchanged. This treatment also lowers the extent of cholinergic muscarinic but not of [3H]naloxone or [3H]spiroperidol binding. In contrast, acrylamide treatment causes major increases of retinal Met-enkephalin and neurotensin concentrations. The binding of [3H]naloxone is also increased, and no reductions of any peptide or binding intensity were observed. The results indicate the plasticity of retinal neuropeptide levels and the selectivity with which these can be modulated.

Acrylamide↗
PubMed1984

Urethane-induced rat retinopathy. Plasticity of the blood-retinal barrier in disease.

Sodium fluorescein and fluoresceinated dextrans penetrate the blood-retinal barrier (BRB) of rats with urethane-induced retinopathy. We have extended these observations, using horseradish peroxidase (HRP) as an ultrastructural probe of the BRB. Intravenous HRP penetrated the BRB 7 weeks after urethane treatment began. This occurred where retinal capillaries invaded the retinal pigment epithelium (RPE) after photoreceptor degeneration. The penetration intensified with duration of the retinopathy, but remained localized near intraepithelial capillaries. The mechanisms by which HRP penetrated the BRB changed as the retinopathy progressed. In the earliest stages (7-10 weeks of age) vesicular transport across endothelia and/or leakage from the choriocapillaris into the pericapillary space of intraepithelial capillaries and then along this space into the retina. At later stages, two more mechanisms were at work: (1) fenestrae developed in the intraepithelial capillaries, and (2) the RPE attenuated, losing its barrier function. Except where this occurred, intercellular RPE junctional complexes remained intact and retarded HRP. We suggest that the rat urethane retinopathy models the plasticity of BRB components--RPE and endothelia--over the course of retinal disease.

Animals↗
PubMedDate not supplied

Abnormal vessel patterns in phototoxic rat retinopathy studied by vascular replicas.

Permeability abnormalities of vessels in rat phototoxic retinopathy have been described for sodium fluorescein and the fluoresceinated dextrans. Since fenestrated vessels within the pigment epithelium (RPE-vessels) had connections to retinal capillaries but not to choroidal vessels, it was presumed that the continuous retinal vessels became fenestrated when located in the abnormal environment of the pigment epithelial cell. It was necessary to rule out a choroidal origin of these unusual RPE-vessels, since they may be a model for other vasculopathies. Vascular cast replicas of whole retinal and choroidal vessel beds from rats with advanced phototoxic retinopathy were studied by scanning electron microscopy. No connection between the retinal and choroidal vasculature was found. Retinal vessels entering the pigment epithelium formed medusa-like coils in local areas. Marked capillary dropout and vessel tortuosity were characteristic. The choroidal capillary bed was normal. This model is appropriate for study of the plasticity of retinal capillaries as seen in diabetic retinopathy and senile macular degeneration.

Animals↗
PubMed2002

Animal models of retinal detachment and reattachment: identifying cellular events that may affect visual recovery.

Retinal detachment continues to be a significant cause of visual impairment, either through the direct effects of macular detachment or through secondary complications such as subretinal fibrosis or proliferative vitreoretinopathy. Animal models can provide us with an understanding of the cellular mechanisms at work that account for the retinopathy induced by detachment and for the generation of secondary effects. As we understand the mechanisms involved, animal models can also provide us with opportunities to test therapeutic agents that may reduce the damaging effects of detachment or improve the outcome of reattachment surgery. They may also reveal information of use to understanding other causes of blindness rooted in retinal defects or injuries. Understanding the effects of detachment (and reattachment) are likely to become even more important as surgeons gain skills in subretinal surgical techniques and macular translocation, both of which will generate short-lived detachments. Here we discuss the fundamental events that occur after detachment, present changes associated with reattachment, and discuss retinal changes that may affect the return of vision.

Animals↗
PubMed2003

Laminar differences in plasticity in area 17 following retinal lesions in kittens or adult cats.

Circumscribed retinal lesions in adult cats result in a reorganization of circuitry in area 17 such that neurons in the lesion projection zone (LPZ) can now be activated, not from their original receptive fields (RFs) but from regions of normal retina adjacent to the lesion ('ectopic' RFs). We have studied this phenomenon further by making circumscribed monocular retinal lesions in 8-week-old kittens and recording responses to visual stimuli of neurons in the LPZ of area 17 when these cats reached adulthood. These responses have been compared with those in adult-lesioned cats either of relatively short postlesion survival (2-24 weeks) or long postlesion survival (3.5-4.5 years). In both kitten-lesioned and adult-lesioned animals most LPZ neurons recorded from the supragranular layers (II and III) not only exhibited new ectopic RFs when stimuli were presented via the lesioned eye but the RF properties (e.g. the sizes of excitatory RFs, orientation and direction selectivities, velocity preferences and upper cut-off velocities) were often indistinguishable from those seen when stimuli were presented via the nonlesioned eye. Similarly, in both kitten-lesioned and adult-lesioned animals, most LPZ neurons recorded from the granular and infragranular layers (IV, V, VI), like those recorded from the supragranular layers, were binocular. However, in adult-lesioned but not in kitten-lesioned animals, the responses and the upper cut-off velocities of LPZ cells recorded from the granular and infragranular layers to stimuli presented via ectopic RFs tended to be, respectively, substantially weaker and lower than those for stimuli presented via the nonlesioned eye. The age-related laminar differences in reorganizational plasticity of cat striate cortex correlate with the lamino-temporal pattern of distribution of N-methyl-d-aspartate glutamate receptors in striate cortex.

Action Potentials↗
PubMed2003

Remodeling of second-order neurons in the retina of rd/rd mutant mice.

This is a brief review of data obtained by analyzing the morphology and the physiology of the retinas in rd/rd and normal, wt mice, aged 10-90 days. Second-order neurons of the rd/rd show abnormalities that start with the anomalous development of rod bipolar cells around P10 and culminate with the atrophy of dendrites in cone bipolar cells, mostly evident at P90. Horizontal cells remodel considerably. Cone-mediated ERGs, (recorded between 13 and 16 days of age) have reduced a-wave and b-wave amplitudes and longer b-wave latency and duration. B-wave abnormalities indicate specific postreceptoral dysfunction. Morphological and ERG changes in rd/rd retinas are consistent with substantial inner retinal remodeling associated to photoreceptor degeneration.

Animals↗
PubMed2000

Investigation of cortical reorganization in area 17 and nine extrastriate visual areas through the detection of changes in immediate early gene expression as induced by retinal lesions.

The effect of binocular central retinal lesions on the expression of the immediate early genes c-fos and zif268 in the dorsal lateral geniculate nucleus (dLGN) and the visual cortex of adult cats was investigated by in situ hybridization and immunocytochemistry. In the deafferented region of the dLGN, the c-fos mRNA level was decreased within 3 days. The dimensions of the geniculate region showing decreased amounts of c-fos mRNA matched the predictions based on the lesion size and the retinotopic maps of Sanderson ([1971] J. Comp. Neurol. 143:101-118). We did not detect zif268 mRNA in the dLGN. At the cortical level, both c-fos and zif268 mRNA expression decreased in the sensory-deprived region of area 17. In addition, the portions of areas 18, 19, 21a, 21b, and 7, as well as the posterior medial lateral suprasylvian area, the posterior lateral lateral suprasylvian area, the ventral lateral suprasylvian area, and the dorsal lateral suprasylvian area corresponding to the retinal lesions also displayed decreased c-fos and zif268 mRNA levels. Immunocytochemistry revealed similar changes for Zif268 and Fos protein. Three days post lesion, the dimensions of the lesion-affected cortical loci exceeded the predictions in relation to the size of the retinal lesions and the available retinotopic maps. Longer postlesion survival times clearly resulted in a time-dependent restoration of immediate early gene expression from the border to the center of the lesion-affected cortical portions. Our findings represent a new approach for investigating the capacity of adult sensory systems to undergo plastic changes following sensory deprivation and for defining the topographic nature of sensory subcortical and cortical structures.

Animals↗
PubMed1997

Retinal protein kinase C.

The protein kinase C (PKC) family of serine/threonine kinase isoenzymes are universally expressed in vertebrate tissues where they control vital cellular functioning. PKC comprises twelve currently identified mammalian isoenzymes, described in three distinct groups according to their need for different effector stimulation. Immunological localisation studies in various vertebrate retinas have indicated the presence, so far, of eight of the PKC subspecies, each with a unique cellular distribution in this tissue. Use of these immunological probing techniques with antibodies raised to the individual PKC family members by immunohistochemistry and western blotting, along with biochemical tools such as the potent activators, the tumour-promoting phorbol esters can hopefully lead to elucidation of the roles of these enzymes in the neural retina. Research work to date has pinpointed a number of roles for PKC in this tissue including control of dopamine release, modulation of glutamate receptor function (probably by a process of direct receptor phosphorylation), phosphorylatory modulation of GABAC-receptor function, an involvement in the retinal ischaemic cascade process (the relevance of which is unknown as yet), involvement in control of cytoskeletal interactions by cytoskeletal element-kinase action and feedback control of enzymes involved in the process of inositol phosphate signalling. PKC has been shown to have an important regulatory role in the process of phototransduction: many of the enzymes and proteins making up the phototransduction cascade act as in vitro and in vivo substrates for PKC-dependent phosphorylation and can have their normal function modified in this way. Also, PKC has been implicated in the control of spinule formation in the retina, a process involved in retinal synaptic plasticity and functioning. All of this work has been described, herein. Collation and utilisation of knowledge of all of the work described here may help us to determine the exact roles for individual isoenzymes in the retina. This in turn may help us to understand and further to prevent pathological conditions leading to inappropriate retinal functioning and possible blindness. Furthermore, understanding the roles of PKC in the neural retina may lead us to vital clues in the understanding of the functioning of this important group of enzymes in the nervous system as a whole and eventually to the prevention of many major neuropathological disorders.

Animals↗