[Technics in the use of fascia lata in retinal detachment surgery].
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Fascia↗
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Results for “retinal plasticity”
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Plastic changes in the distribution and soma size of retinal ganglion cells after neonatal monocular enucleation in rats.
Using the method of retrograde labeling of ganglion cells with HRP, we studied in adult rats the plastic changes in the retinogeniculate projections due to monocular enucleations shortly after birth. Four normal and 6 neonatally enucleated rats were used. In two of the normal and 4 of the enucleated rats a small amount of HRP was injected into the dorsal lateral geniculate nucleus (LGd) and in 4 other rats massive injections were made into the optic tract near the LGd. Neonatally unilaterally eye-enucleated rats were characterized by an expanded distribution of ipsilaterally projecting ganglion cells all over the retina of the remaining eye and by a densely packed distribution of these cells in the lower temporal retina in which area these cells have only a moderate density in normal rats. On the contrary, in the lower temporal retina of monocularly enucleated rats the incidence of contralaterally projecting ganglion cells was decreased. Soma areas of ipsi- and contralaterally projecting ganglion cells were measured for the peripheral crescent in lower temporal and lower nasal retinas. As compared with normal rats, neonatally enucleated rats had a larger mean soma area of ipsilaterally projecting cells and a smaller mean soma area of contralaterally projecting cells. This result was interpreted as suggesting that after neonatal monocular enucleation medium to large cells had changed their side of axonal projection from the contralateral to ipsilateral LGd.
Animals↗
Synaptic plasticity in mammalian photoreceptors prepared as sheets for retinal transplantation.
PURPOSE: To investigate systematically the early morphologic changes in axon terminals of adult mammalian rod and cone photoreceptors prepared as a sheet for subretinal transplantation. METHODS: An in vitro system was designed to maintain adult porcine retinas for up to 48 hours. Photoreceptor sheets, prepared by vibratome sectioning, and full-thickness retinas were cultured at temperatures similar to those in pretransplantation storage (4 degrees C) and after transplantation (37 degrees C). Changes in the outer nuclear and outer plexiform layers were analyzed, using immunohistochemistry, laser scanning confocal microscopy, and image analysis. RESULTS: Morphologic changes were observed in photoreceptor sheets as early as 10 minutes after incubation. The most significant change was the retraction of photoreceptor axons and terminals toward their cell bodies. Retraction was temperature dependent, being exacerbated at 37 degrees C compared with 4 degrees C, at its maximum by 24 hours of culture, and present in sheets obtained from both superior and inferior retina. The cause of this movement was not preparation techniques associated with vibratome sectioning or gelatin removal. Retraction was also present in full-thickness neural retina incubated at 37 degrees C. Reduction in outer nuclear layer cell counts and thickness were also evident in these preparations, primarily in photoreceptor sheets. CONCLUSIONS: Adult photoreceptor sheets, a potential graft preparation for retinal transplantation, show a rapid retraction of axon terminals toward the cell bodies during culture. Although retraction may impede synaptic integration after transplantation, this intrinsic plasticity could be redirected to stimulate graft-host interaction.
Animals↗
Neural remodeling in retinal degeneration.
Mammalian retinal degenerations initiated by gene defects in rods, cones or the retinal pigmented epithelium (RPE) often trigger loss of the sensory retina, effectively leaving the neural retina deafferented. The neural retina responds to this challenge by remodeling, first by subtle changes in neuronal structure and later by large-scale reorganization. Retinal degenerations in the mammalian retina generally progress through three phases. Phase 1 initiates with expression of a primary insult, followed by phase 2 photoreceptor death that ablates the sensory retina via initial photoreceptor stress, phenotype deconstruction, irreversible stress and cell death, including bystander effects or loss of trophic support. The loss of cones heralds phase 3: a protracted period of global remodeling of the remnant neural retina. Remodeling resembles the responses of many CNS assemblies to deafferentation or trauma, and includes neuronal cell death, neuronal and glial migration, elaboration of new neurites and synapses, rewiring of retinal circuits, glial hypertrophy and the evolution of a fibrotic glial seal that isolates the remnant neural retina from the surviving RPE and choroid. In early phase 2, stressed photoreceptors sprout anomalous neurites that often reach the inner plexiform and ganglion cell layers. As death of rods and cones progresses, bipolar and horizontal cells are deafferented and retract most of their dendrites. Horizontal cells develop anomalous axonal processes and dendritic stalks that enter the inner plexiform layer. Dendrite truncation in rod bipolar cells is accompanied by revision of their macromolecular phenotype, including the loss of functioning mGluR6 transduction. After ablation of the sensory retina, Müller cells increase intermediate filament synthesis, forming a dense fibrotic layer in the remnant subretinal space. This layer invests the remnant retina and seals it from access via the choroidal route. Evidence of bipolar cell death begins in phase 1 or 2 in some animal models, but depletion of all neuronal classes is evident in phase 3. As remodeling progresses over months and years, more neurons are lost and patches of the ganglion cell layer can become depleted. Some survivor neurons of all classes elaborate new neurites, many of which form fascicles that travel hundreds of microns through the retina, often beneath the distal glial seal. These and other processes form new synaptic microneuromas in the remnant inner nuclear layer as well as cryptic connections throughout the retina. Remodeling activity peaks at mid-phase 3, where neuronal somas actively migrate on glial surfaces. Some amacrine and bipolar cells move into the former ganglion cell layer while other amacrine cells are everted through the inner nuclear layer to the glial seal. Remodeled retinas engage in anomalous self-signaling via rewired circuits that might not support vision even if they could be driven anew by cellular or bionic agents. We propose that survivor neurons actively seek excitation as sources of homeostatic Ca(2+) fluxes. In late phase 3, neuron loss continues and the retina becomes increasingly glial in composition. Retinal remodeling is not plasticity, but represents the invocation of mechanisms resembling developmental and CNS plasticities. Together, neuronal remodeling and the formation of the glial seal may abrogate many cellular and bionic rescue strategies. However, survivor neurons appear to be stable, healthy, active cells and given the evidence of their reactivity to deafferentation, it may be possible to influence their emergent rewiring and migration habits.
Animals↗
N-methyl-D-aspartate (NMDA)--induced apoptosis in rat retina.
PURPOSE: The involvement of apoptosis in N-methyl-D-aspartate (NMDA)-induced excitotoxicity in adult rat retinas was examined. METHODS: Excitotoxic loss of inner retinal elements was induced by intravitreal injections of various concentrations of neutralized NMDA in adult albino Lewis rats. Tissue responses were quantified by measuring the inner retinal thickness (IRT) in plastic sections of the retinas and cell counts in the retinal ganglion cell layer in flatmount preparations of the whole retinas. Internucleosomal DNA fragmentation, a hallmark of apoptosis, was assayed with agarose DNA gel electrophoresis. The in situ TdT-mediated biotin-dUTP nick end labeling (TUNEL) method was used to locate nicked DNA in paraffin sections of the retinas. Ultrastructural changes of the degenerating cells were examined by electron microscopy. The efficacy of Ac-Tyr-Val-Ala-Asp-CMK (YVAD-CMK), a peptidyl caspase inhibitor, and 3-aminobenzamide (ABA), an inhibitor of poly(ADP-ribose) polymerase (PARP), in ameliorating the loss of inner retinal elements was evaluated using morphometry to examine the apoptotic pathways. RESULTS: Intravitreal injection of NMDA induced a dose-dependent loss of inner retinal elements as evidenced by the measurements of IRT and RGCCs. There were time- and dose-related appearances of internucleosomal fragmentation of retinal DNA and a time-related appearance of TUNEL-positive nuclei in the inner retinas after intravitreal NMDA injection. Ultrastructural features consistent with classic apoptotic changes were noted in degenerating cells in the retinal ganglion cell layer and the inner nuclear layer. Control retinas given vehicle, N-methyl-L-aspartate (the L-isomer of NMDA), or NMDA plus MK-801, a specific antagonist, did not show these changes. Simultaneous administration of NMDA and YVAD-CMK or ABA abolished or attenuated the loss of RGCCs in the posterior retinas. CONCLUSIONS: NMDA-induced excitotoxicity involved apoptosis and caspases and PARP may play important roles in the pathways.
Amino Acid Chloromethyl Ketones↗
Experience-dependent mechanism of binocular map plasticity in Xenopus: incongruent connections are masked by retinal input.
When one eye in larval Xenopus is rotated to change the orientation of its visual map on the contralateral tectum, the map from the other eye to the same tectum can subsequently alter its orientation to match the rotated input. This plasticity re-establishes binocular congruence between the two maps and involves an experience-dependent reorganization of functional connections in the crossed isthmotectal projection, which delivers the ipsilateral eye's map to the tectum. Here, recordings were made at the same tectal sites in 8 eye-rotated frogs immediately before and after removing the rotated retina. All had congruent binocular maps prior to enucleation, with matching receptive fields in the two eyes at each recording site. In 5 frogs, eye removal unmasked additional, incongruent receptive fields in the ipsilateral eye, recorded from previously undetectable crossed isthmotectal connections occupying their original positions in the tectum. This result suggests that the plasticity also involves functional suppression of binocularly-incongruent inputs from the ipsilateral eye by retinotectal afferents.
Animals↗
Selective alterations in glutamate receptor subtypes after unilateral orbital enucleation.
Glutamate is the major excitatory neurotransmitter in the rat visual system. Using quantitative autoradiography the effect of unilateral orbital enucleation on [3H]kainate, [3H]alpha-amino-3-hydroxy-5-methyl- isoxazole-4-propionic acid [( 3H]AMPA) and [3H]glutamate binding to kainate, quisqualate and NMDA receptors respectively has been examined within anatomical components of the visual pathway at 4 time points up to 20 days post-lesion. The time course for the degeneration of retinal projection fibres was assessed in a separate group of animals by quantifying [3H]cyclohexyladenosine [( 3H]CHA) binding to presynaptic adenosine A1 receptors. Over the first 5 days after orbital enucleation, there were no significant alterations in glutamate or adenosine A1 receptor binding in visual structures of the visually deprived hemisphere. However, at 10 days post-lesion [3H]AMPA binding was significantly reduced (30%) in the visually deprived superior colliculus but unaltered in other visual structures. At this time point there was also a significant reduction (50%) in [3H]CHA binding in the visually deprived superior colliculus but not in other retino-recipient nuclei. There were similar changes in [3H]AMPA and [3H]CHA binding at 20 days post-enucleation. [3H]Kainate binding was significantly increased in the visually deprived superior colliculus only at 20 days post-enucleation. Saturation analysis of [3H]kainate and [3H]AMPA binding at this time point indicated a selective increase in the Bmax value for the high affinity [3H]kainate binding site and a concomitant decrease in the Bmax value for the high affinity [3H]AMPA binding site in the visually deprived superior colliculus. There were, however, no significant alterations in [3H]AMPA or [3H]kainate binding in other primary projection areas or in secondary visual areas (e.g. visual cortex) at any time point. NMDA sensitive [3H]glutamate binding was unaltered in the visually deprived hemisphere up to 20 days post-enucleation. These results suggest an upregulation of kainate receptors in the visually deprived superior colliculus after orbital enucleation and a loss of presynaptic quisqualate receptors on degenerating retinal fibres. The plastic alterations in kainate receptors in the superior colliculus are supportive of electrophysiological data suggesting a physiological role for these sites in mediating excitatory postsynaptic potentials in tectal neurons.
Animals↗
Retinal axon guidance: near or far?
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Animals↗
A method for spatio-temporal (4-D) data representation in confocal microscopy: application to neuroanatomical plasticity.
This paper describes a new method for data representation and visualization in four dimensions (three dimensions plus time). Sequential volumes, exhibiting morphological activity, are acquired non-invasively with a confocal scanning laser microscope, where each data set corresponds to a time sample. A pipelined processing includes packing of volumes and specific volume rendering techniques. Subsequent processing in HIS (hue, intensity, saturation)l colour space combines functional, packed images with shaded three-dimensional views. As a result, even subtle changes in morphology become visible and computational time is saved. Experimental findings obtained from investigations of synaptic plasticity in cultured retinal tissue are reported.
Algorithms↗
A role for retinal brain-derived neurotrophic factor in ocular dominance plasticity.
Visual deprivation is a classical tool to study the plasticity of visual cortical connections. After eyelid closure in young animals (monocular deprivation, MD), visual cortical neurons become dominated by the open eye, a phenomenon known as ocular dominance (OD) plasticity . It is commonly held that the molecular mediators of OD plasticity are cortically derived and that the retina is immune to the effects of MD . Recently, it has been reported that visual deprivation induces neurochemical, structural, and functional changes in the retina , but whether these retinal changes contribute to the effects of MD in the cortex is unknown. Here, we provide evidence that brain-derived neurotrophic factor (BDNF) produced in the retina influences OD plasticity. We found a reduction of BDNF expression in the deprived retina of young rats. We compensated this BDNF imbalance between the two eyes by either injecting exogenous BDNF in the deprived eye or reducing endogenous BDNF expression in the nondeprived eye. Both treatments were effective in counteracting the OD shift induced by MD. Retinal BDNF could also influence OD distribution in normal animals. These results show for the first time that OD plasticity is modulated by BDNF produced in the retina.
Analysis of Variance↗
Retinal image quality during oblique gaze through spectacle lenses: plastic vs. glass.
The optical performance of standard plastic and glass spectacle lenses was compared at increasing angles of oblique gaze up to 40 degrees on either side of the optic axis of the lenses. For this purpose, the border enhancement method was used, a method which is suitable for monitoring small order changes in the retinal image. It was found that the enhancement band width increases with obliquity of gaze in all cases, signifying a deterioration in the retinal image. A glass lens will exaggerate this deterioration to some extent, whereas a plastic lens will exaggerate it to the greatest extent. It is shown that the relatively poorer performance of plastic is due to a relatively larger amount of narrow-angle scattering than is produced by glass.
Eyeglasses↗
[Bioplast implant. New surgical method in retinal detachment. Preliminary report].
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Humans↗
Müller cell and neuronal remodeling in retinal detachment and reattachment and their potential consequences for visual recovery: a review and reconsideration of recent data.
Recent evidence suggests that the adult mammalian retina is far more plastic than was previously thought. Retinal detachment induces changes beyond the degeneration of outer segments (OS). Changes in photoreceptor synapses, second- and even third-order neurons may all contribute to imperfect visual recovery that can occur after successful reattachment. Changes that occur in Müller cells have obvious effects through subretinal fibrosis and proliferative vitreoretinopathy, but other unidentified effects seem likely as well. Reattachment of the retina induces its own set of responses aside from OS re-growth. Reattachment halts the growth of Müller cell processes into the subretinal space, but induces their growth on the vitreal surface. It also induces the outgrowth of rod axons into the inner retina.
Animals↗
Role of the flocculus of the cerebellum in motor learning of the vestibulo-ocular reflex.
Structure-function studies at the systems level are an effective method for understanding the relationship of the central nervous system to behavior. Motor learning or adaptation of the vestibulo-ocular reflex is a clear example wherein this approach has been productive. During a vestibulo-ocular reflex the brain converts a head velocity signal, transduced through the vestibular semicircular canals, into an eye movement command delivered to the extraocular muscles. If the viewed target remains on the fovea of the retina, the reflex is compensatory, and its gain, eye velocity/head velocity, is one. When the image of the viewed object slips across the retina, visual acuity decreases, and the gain of the reflex, which is no longer one, is plastically adapted or adjusted until retinal stability is restored. The anatomic substrate for this plasticity thus involves brain structures in which visual-vestibular interaction can potentially occur, as well as vestibular and visual sensory and oculomotor motor structures. Further, it has been known for many years that removal of the flocculus of the cerebellum permanently precludes further vestibulo-ocular reflex adaptation, demonstrating the involvement of the cerebellum in this behavior. Maekawa and Simpson (J Neurophysiol 1973;36: 649-66) discovered that one visual input to the flocculus involved the accessory optic system and the inferior olive. Ensuing work has demonstrated that the visual signals used to adapt the vestibulo-ocular reflex are transmitted by this accessory optic system to the flocculus and subsequently to brain stem structures involved in vestibulo-ocular reflex plasticity. Presently the inclusive list of anatomic sites involved in vestibulo-ocular reflex circuitry and its adaptive plasticity is small. Our laboratory continues to believe that this behavior should be caused by interactions within this small class of neurons. By studying each class of identified neuron and its interactions with others within the list, we hope to ultimately understand the mechanisms used by the brain in the expression of this behavior.
Adaptation, Physiological↗
Differential modulation of light-evoked on- and off-EPSCs by paired-pulse stimulation in salamander retinal ganglion cells.
Short-term plasticity of On- and Off-EPSPs, and its potential role in regulation of signal processing was studied in salamander retinal On-Off ganglion cells by whole-cell recording. Paired-pulse light stimulation resulted in a depression of On-, and an enhancement of Off-EPSCs. Recovery from depression and enhancement was exponential and complete by 20 s. Paired-pulse enhancement, but not depression, was abolished with increasing stimulus duration. Blockade of On-EPSC by L-2-amino-4-phosphonobutyrate (AP-4), an agonist at group III mGluRs, significantly increased Off-EPSCs evoked by short (<2 s) duration conditioning light stimuli, resulting in a reversal of the paired-pulse enhancement to depression. The acetylcholinesterase inhibitor eserine reduced Off-EPSC1 and increased the ratio of enhancement. An opposite effect was observed in the presence of the nACh receptor antagonist d-tubocurarine. AP-7, an antagonist of NMDA receptors attenuated the enhancement of Off-EPSCs. In current clamp mode paired-pulse stimulation resulted in a modulation of light evoked, as well as the depolarization-induced spike firing pattern of ganglion cells. The present study suggests that paired light stimulation differently modulates On and Off EPSPs, and the light-evoked spike firing pattern of On-Off ganglion cells.
Action Potentials↗
[ON VARIOUS METHODS OF SCLERAL REINFORCEMENT UTILIZABLE IN RETINAL DETACHMENT SURGERY].
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Choroid↗
Transient up-regulation of the rostrocaudal gradient of ephrin A2 in the tectum coincides with reestablishment of orderly projections during optic nerve regeneration in goldfish.
During development, a graded expression of ephrin A2 has been implicated in retinotectal map formation. Here we have examined ephrin A2 expression during optic nerve regeneration in the mature goldfish. In the tecta of normal animals, a gradient of ephrin A2 expression is detected in cell bodies within the stratum fibrosum et griseum superficiale with more immunopositive cells caudally than rostrally. The gradient in the mature animal presumably reflects the plasticity associated with continued retinal and tectal neurogenesis. During optic nerve regeneration, expression throughout the tectum is increased by 1 month as a strong rostrocaudal gradient. The gradient declines to normal by 3 months. The up-regulation of ephrin A2 during optic nerve regeneration is likely to be instrumental in reestablishing the retinotectal map.
Animals↗
Development of dendritic trees of rabbit retinal alpha ganglion cells: relation to differential retinal growth.
To provide a quantitative description of the postnatal development of dendritic trees in alpha ganglion cells of the rabbit retina, these cells were stained either by intracellular injection of Lucifer yellow or by application of the lipophilic dye DiI. This was done at three developmental stages: postnatal day (P) 8/9, P 16/17, and in adults. For different retinal locations we quantified the alpha cell dendritic field area, the number of dendritic branch points, and the average dendritic length between branch points. According to the alpha cell location, the data were collected in three groups representing the retinal center, midperiphery, and far periphery, respectively. The data were then correlated with the postnatal retinal expansion which is known to differ among the above topographic regions of the retinae (Reichenbach et al., 1993). Our results show that the growth of alpha ganglion cell dendrites is not proportional to, but significantly exceeds, that of the local retinal tissue. Between P 8/9 and adulthood, the area of central alpha cells increases almost six-fold from 26,000 to 144,000 microns 2 (retinal expansion: 2.2-fold), and that of peripheral cells more than 15-fold from 35,000 to 556,000 microns 2 (retinal expansion: four-fold). During this period, the coverage factor of alpha cell dendritic fields increases about three-fold, and reaches adult levels of about 3 (retinal center) and 2.2 (periphery), respectively. The number of dendritic branch points remains nearly constant, and the distance between them increases by a factor close to the square root of the factor by which the dendritic field area grows. Thus, it appears that, from the second postnatal week on, dendritic trees of rabbit alpha ganglion cells increase by intense "interstitial growth," rather than by outgrowth of (new) dendritic branches. This growth pattern is different from that of some other rabbit retinal ganglion cell types, and of alpha ganglion cells of the cat retina, whose dendritic trees expand at a rate equal to or less than that of the surrounding retinal tissue. The consequences for synaptic contacts with bipolar and amacrine cells are discussed; they suggest a high degree of synaptic plasticity during normal postnatal retinal growth.
Animals↗