Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “retinal plasticity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources

Fine structure of the pecten oculi in the great horned owl (Bubo virginianus).

The pecten oculi of the great horned owl (Bubo virginianus) has been examined by light and electron microscopy. The pecten in this species is of the pleated type and is small in comparison to the size of the eyeball. It consists of 7-8 accordion folds which are joined apically by a pigmented bridge of tissue. Within each fold are numerous capillaries, larger supply and drainage vessels and plentiful pleomorphic melanocytes. The capillaries are extremely specialized vessels, most of which display plentiful microfolds on both their luminal and abluminal surfaces although some capillaries show but a few microfolds. The endothelial cell bodies are extremely thin with most organelles located near the nucleus. All capillaries are surrounded by a thick fibrillar basal lamina which is felt to be structurally important. Pericytes are a common feature within these thickened basal laminae. The numerous melanocytes form an incomplete sheath around the capillaries and are also presumed to be fulfilling a structural role. While the morphology of the pecten in the great horned owl is certainly indicative of a heavy involvement in transport, when compared to the pecten in species that are more visually oriented it is smaller, displays fewer folds and a reduced number of microfolds within the capillaries.

Animals↗

Regulation of structural plasticity by different channel types in rod and cone photoreceptors.

In response to retinal disease and injury, the axon terminals of rod photoreceptors demonstrate dramatic structural plasticity, including axonal retraction, neurite extension, and the development of presynaptic varicosities. Cone cell terminals, however, are relatively inactive. Similar events are observed in primary cultures of salamander photoreceptors. To investigate the mechanisms underlying these disparate presynaptic responses, antagonists to voltage-gated L-type and cGMP-gated channels, known to be present on rod and cone cell terminals, respectively, were used to block calcium influx during critical periods of plasticity in vitro. In rod cells, L-type channel antagonists nicardipine and verapamil inhibited not only the outgrowth of processes and the formation of varicosities, but also the synthesis of vesicle proteins, SV2 and synaptophysin. In contrast, the synthesis of opsin in rod cells was unaffected. In cone cells, L-type channel antagonists caused only modest changes. However, cobalt bromide, which blocks all calcium channels, and l-cis-diltiazem, a potent antagonist of cGMP-gated channels, significantly inhibited varicosity formation and synthesis of SV2 in cone cells. Moreover, the cGMP-gated channel agonist 8-bromo-cGMP caused a significant increase in varicosity formation by cone but not rod cells. Thus voltage-gated L-type channels in rod cells and cGMP-gated channels in cone cells are the primary calcium channels required for structural plasticity and the accompanying upregulation of synaptic vesicle synthesis. The differing responses of rod and cone terminals to injury and disease may be determined by these differences in the regulation of Ca2+ influx.

Ambystoma↗

Coupling an aVLSI neuromorphic vision chip to a neurotrophic model of synaptic plasticity: the development of topography.

We couple a previously studied, biologically inspired neurotrophic model of activity-dependent competitive synaptic plasticity and neuronal development to a neuromorphic retina chip. Using this system, we examine the development and refinement of a topographic mapping between an array of afferent neurons (the retinal ganglion cells) and an array of target neurons. We find that the plasticity model can indeed drive topographic refinement in the presence of afferent activity patterns generated by a real-world device. We examine the resilience of the developing system to the presence of high levels of noise by adjusting the spontaneous firing rate of the silicon neurons.

Models, Neurological↗

Choroidal microvascular repair after argon laser photocoagulation.

We studied the repair process of the choriocapillaris after argon laser retinal photocoagulation in the domestic cat with a plastic injection-corrosion technique and scanning electron microscopy. Retinal scatter photocoagulation was applied to the tapetum at threshold-, moderate-, and high-intensity levels and specimens prepared one, ten, and 30 days later. At 24 hours after photocoagulation, obstruction of the choriocapillaris was always present regardless of the power used. In lesions produced by higher-intensity energy levels, choriocapillaris defects had larger diameters and larger vessels were affected more severely. At ten days, there were early signs of choriocapillaris repair. At 30 days, choriocapillaris occupied almost the entire area of the defect, although the normal lobular architecture was not present.

Animals↗

Topographic map reorganization in cat area 17 after early monocular retinal lesions.

Neither discrete peripheral retinal lesions nor the normal optic disk produces obvious holes in one's percept of the world because the visual brain appears to perceptually "fill in" these blind spots. Where in the visual brain or how this filling in occurs is not well understood. A prevailing hypothesis states that topographic map of visual cortex reorganizes after retinal lesions, which "sews up" the hole in the topographic map representing the deprived area of cortex (cortical scotoma) and may lead to perceptual filling in. Since the map reorganization does not typically occur unless retinotopically matched lesions are made in both eyes, we investigated the conditions in which monocular retinal lesions can induce comparable map reorganization. We found that following monocular retinal lesions, deprived neurons in cat area 17 can acquire new receptive fields if the lesion occurred relatively early in life (8 weeks of age) and the lesioned cats experienced a substantial period of recovery (>3 years). Quantitative determination of the monocular and binocular response properties of reactivated units indicated that responses to the lesioned eye for such neurons were remarkably robust, and that the receptive-field properties for the two eyes were generally similar. Moreover, excitatory or inhibitory binocular interactions were found in the majority of experimental units when the two eyes were activated together. These results are consistent with the hypothesis that map reorganization after monocular retinal lesions require experience-dependent plasticity and may be involved in the perceptual filling in of blind spots due to retinal lesions early in life.

Animals↗

Morphology of retinal axons induced to arborize in a novel target, the medial geniculate nucleus. I. Comparison with arbors in normal targets.

Ferret retinal axons can be induced to innervate the medial geniculate nucleus (MGN) by a combination of brain lesions early in development. Our previous work suggests that the retinal ganglion cells responsible for this plasticity are W cells. The present study continues this work with a morphological investigation of normal retinal ganglion-cell axons and retinal ganglion-cell axons induced to arborize in the MGN. Retinal axons were bulk filled with horseradish peroxidase placed in the optic tract, and individual axons were serially reconstructed from sagittal sections. The control population consisted of fine-caliber axons arborizing in the superior colliculus (SC) and in the ventral C laminae of the lateral geniculate nucleus (LGN) of normal ferrets. We also compared the axons in the MGN of lesioned ferrets to intracellularly filled X and Y axons from normal ferrets as reported by Roe et al. ([1989] J. Comp. Neurol. 288:208). We have found that the retino-MGN axons in the lesioned ferrets do not resemble X or Y axons in normal ferrets in axon diameter, arbor volume, bouton number, or bouton density. However, they do resemble the fine-caliber, presumed W axons arborizing in the C laminae of the LGN and in the SC of normal ferrets. Thus, this study, in combination with previous studies, suggests strongly that W retinal ganglion cells are responsible for the retinal input to the MGN in lesioned animals. In addition, we find that the retino-MGN axons are of two types, branched and unbranched, which may correspond to different subtypes of retinal W cells.

Animals↗

Evidence for a threshold in experience-dependent long-term changes of kitten visual cortex.

In order to determine the role of unstructured and of spontaneous activity in the developmental plasticity of the visual cortex, we blocked in 7 kittens the retinal activity of one eye completely by intraocular injections of tetrodotoxin (TTX) while the other eye was left open. Littermates of these kittens were monocularly deprived by lid suture and served as controls. In 3 additional kittens one eye was inactivated with TTX and the other closed by lid suture to assess whether mere asymmetries in the activation levels of the two eyes were sufficient to induce ocular dominance changes. Despite some variability between the matched pairs, the ocular dominance shift towards the normal eye did not differ significantly in the kittens with monocular lid suture and monocular TTX injection (P greater than 0.3/chi 2). In the TTX-treated kittens there was a trend for neurones to be less sharply tuned for orientation but it was not significant (P greater than 0.08/chi 2). In the kittens which had one eye injected with TTX and the other sutured closed no shift of ocular dominance was apparent. Separate analysis of both hemispheres revealed only a small bias towards the respective contralateral eye. We conclude that the process mediating activity-dependent long-term changes of ocular dominance has a threshold. Afferent activity that fails to excite the postsynaptic neuron above this threshold plays neither a significant role in the stabilization nor in the disruption of functional connections.

Animals↗

Protection of the rat retina from ischemic injury by brain-derived neurotrophic factor, ciliary neurotrophic factor, and basic fibroblast growth factor.

PURPOSE: The protective effects of three survival-promoting agents on ischemia-induced retinal injury in the rat were investigated. The agents included brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), and basic fibroblast growth factor (bFGF). METHODS: Retinal ischemia was induced in Lewis albino rats by increasing intraocular pressure to 160 mm Hg for 90 minutes. The agents or buffer controls were injected intravitreally at different times, either before or after the ischemic insult, and the postischemic survival time was either 7 or 14 days. The degree of retinal damage was assessed from plastic-embedded sections by cytologic analysis, measurement of the thickness of several layers, and neuronal counts of the ganglion cell layer. RESULTS: Retinal ischemia thinned and reduced cell numbers in the inner retinal layers, but not in the photoreceptor nuclear layer. Each agent transiently ameliorated the degenerative changes when it was injected 2 days before ischemia. At 7 days postischemia, the inner retinal layers were far less damaged, and more ganglion cells were present than in buffer-injected or uninjected eyes. The protective effect was no longer evident at 14 days postischemia, except in the inner nuclear layer of the BDNF-treated eyes. If a second injection of BDNF was made 5 days after the ischemic insult, then the inner retinal layers were more preserved than buffer controls at 14 days postischemia, but the survival of ganglion cells was not enhanced. A single injection of BDNF at either 1 or 3 days postischemia reduced the degree of inner retinal damage and increased the number of surviving ganglion cells over that in buffer-injected controls. (CNTF and bFGF were not studied with postischemic injections.) CONCLUSIONS: BDNF, CNTF, and bFGF transiently protect the retina from pressure-induced ischemic injury when given 2 days before ischemia, and a second injection of BDNF given postischemically can prolong the protective effect. Moreover, protection afforded by BDNF can be seen even when applied only 1 or 3 days after the ischemic insult, although the protective effect is greater at 1 day than at 3 days postischemia.

Animals↗

The study of influencing factors on the growth characters of Sprague-Dawley rat retinal neurons in vitro.

PURPOSE: To investigate the influencing factors in culturing Sprague-Dawley (S-D) rats retinal neurons in order to lay foundation for further experimental research. MATERIALS AND METHODS: Retinal cells were plated on plastic plates and coverslips coated with poly-l-lysine or ethylene imine polymer for primary culture. The cultured cells were divided into following groups: 1. Culture medium changed every 2 to 3 days vs changed only once; 2. Cytosine arabinoside (Ara-C) added to the culture medium vs not added. The cells were observed and pictured under inverted phase contrast microscope. The cells were identified through immunocytochemistry. RESULTS: The immunofluorescence showed that most of the cultured cells were neurons, among them were a few retinal ganglion cells. In the cultured group of which substrata coated with poly-l-lysine and culture medium added with Ara-c, the neurons intended to aggregate into clusters with relatively straight neurites. In the group of which substrata coated with ethylene imine polymer and medium added with Ara-c, the neurons grew dispersively with bent neurites. Both of them survived for 2 to 3 weeks. The cells which plated in the medium not added with Ara-c did not aggregate into clusters and survived longer than 4 weeks. In the group of which medium changed several times, the survival time of neurons was shorter than that in the medium changed only once. CONCLUSIONS: The retinal neurons plated on the substrata coated with ethylene imine polymer are easy to observe because of its dispersive growth. It is not favorable for the growth of the neurons by changing culture medium many times. Ara-c may possibly have side effect on the growth of retinal neurons.

Animals↗

Lithium reduces ocular dominance plasticity in kitten visual cortex.

Activity-dependent processes within the visual pathway play a crucial role in the expression of ocular dominance plasticity in immature visual cortex. The necessity of non-retinal, modulatory afferents to the regulation of ocular dominance plasticity has been recognized. Among a few chemically defined signaling systems, the noradrenaline-activated beta-adrenoreceptors seem to have a prime role in this matter. The involvement of acetylcholine afferents was also proven. We looked for plausible molecular mechanisms which integrate the contribution of the two neuromodulator systems to ocular dominance plasticity. At the first step, based on the rich literature on psychotropic action of lithium and the recent advancement in understanding of its molecular mechanisms, we physiologically studied visual cortex of kittens which had been repeatedly injected with the lithium solution intraperitoneally or the cortex directly infused with it. We found (1) that ocular dominance plasticity was significantly reduced in lithium-injected kittens, (2) that the decrease was directly correlated with plasma concentrations of lithium (i.e. the higher the lithium concentration, the lower the plasticity), and (3) that the comparable decrease in the plasticity was obtained from kitten visual cortex which had been directly infused with the lithium solution. The present results suggest that lithium-sensitive processes, through most likely reduced production of second messengers, underlie the regulation of ocular dominance plasticity.

Animals↗

Neurochemical heterogeneity of retinal bipolar cells.

BACKGROUND: Retinal bipolar cells show neurochemical changes in response to retinal insult, which could have profound effects on retinal function or recovery after insult however, the neurochemistry of bipolar cells is incompletely understood. METHODS The distribution of the amino acid neurotransmitters glutamate, gamma-aminobutyric acid (GABA), and glycine, and the metabolic amino acids, aspartate and glutamine, was examined immunocytochemically in the retina of the tiger salamander, a major model for the study of retinal anatomy and function. RESULTS: Each amino acid showed a unique distribution among retinal bipolar cells. All bipolar cells appear to contain glutamate and, under appropriate conditions, may also contain aspartate. GABA and glycine were restricted to a subset of conventionally placed bipolar cells located in the inner nuclear layer, but were not present in displaced bipolar cells located in the outer nuclear layer. In contrast, high levels of glutamine were almost exclusively restricted to displaced bipolar cells. Analysis of co-localization patterns revealed several different amino acid signatures within the bipolar cell population. CONCLUSIONS: The striking neurochemical heterogeneity among bipolar cells suggests important differences in signaling and metabolism that could affect cell survival, plasticity, and functional recovery from retinal insult in a cell-type-specific manner.

Ambystoma↗

Spatial integration and cortical dynamics.

Cells in adult primary visual cortex are capable of integrating information over much larger portions of the visual field than was originally thought. Moreover, their receptive field properties can be altered by the context within which local features are presented and by changes in visual experience. The substrate for both spatial integration and cortical plasticity is likely to be found in a plexus of long-range horizontal connections, formed by cortical pyramidal cells, which link cells within each cortical area over distances of 6-8 mm. The relationship between horizontal connections and cortical functional architecture suggests a role in visual segmentation and spatial integration. The distribution of lateral interactions within striate cortex was visualized with optical recording, and their functional consequences were explored by using comparable stimuli in human psychophysical experiments and in recordings from alert monkeys. They may represent the substrate for perceptual phenomena such as illusory contours, surface fill-in, and contour saliency. The dynamic nature of receptive field properties and cortical architecture has been seen over time scales ranging from seconds to months. One can induce a remapping of the topography of visual cortex by making focal binocular retinal lesions. Shorter-term plasticity of cortical receptive fields was observed following brief periods of visual stimulation. The mechanisms involved entailed, for the short-term changes, altering the effectiveness of existing cortical connections, and for the long-term changes, sprouting of axon collaterals and synaptogenesis. The mutability of cortical function implies a continual process of calibration and normalization of the perception of visual attributes that is dependent on sensory experience throughout adulthood and might further represent the mechanism of perceptual learning.

Animals↗

Detailed histopathologic characterization of the retinopathy, globe enlarged (rge) chick phenotype.

PURPOSE: The purpose of this study was to characterize the morphological abnormalities in the retinas of chicks (Gallus gallus) suffering from the autosomal recessive disease, retinopathy, globe enlarged (rge/rge). METHODS: rge/rge affected and age matched control retinas were examined from hatch up to 730 days of age. Thickness of retinal layers at six retinal regions was measured from plastic embedded sections. Morphological features were examined on semi-thin sections by light microscopy and on ultra-thin sections by transmission electron microscopy. Immunohistochemistry was performed using a panel of several different antibodies. Additionally, comparative counting of rod outer segments, rows of cells in the inner nuclear layer, and ganglion cells per unit length was performed. RESULTS: The earliest changes observed in rge/rge retinas were disorganization of the outer plexiform layer and abnormal location of the endoplasmic reticulum of the photoreceptors. In rge/rge retinas, cone pedicles were larger, irregular in shape, and usually contained multivesicular bodies. In addition, synaptic ribbons of the cone pedicles and rod spherules in rge/rge retinas were less numerous compared to controls. Large glycogen deposits progressively accumulated in the perinuclear cytoplasm associated with the abnormally located endoplasmic reticuli in accessory cones and rods. Total retinal thickness progressively decreased with age in rge/rge birds. This was accompanied by a decrease in the number of cells in the inner nuclear layer and a decrease in the number of rod outer segments (OSs). Several changes were detected in the rge/rge retinas using immunohistochemistry, including mislocalized opsin immunoreactivity of rod photoreceptors, a decrease in number and disorganization of opsin positive rod OSs (especially in the peripheral regions), a decrease in number of tyrosine hydroxylase positive neurites in the distal inner plexiform layer, and activation of macroglial and microglial cells. CONCLUSIONS: As we previously reported, the rge/rge chick has vision loss that is not the result of photoreceptor loss and is unusual in that electroretinographic responses, although abnormal, are maintained until well after vision loss has developed. The phenotype is associated with a developmental disruption of both rod and cone photoreceptor synaptic terminals that progresses with age. It is possible that these changes may be indicative of abnormal circuitry within the outer plexiform layer, and that they underlie the progressive loss of vision in rge/rge birds. Other early changes suggesting photoreceptor abnormality are dilation of photoreceptor cell bodies, abnormal positioning of endoplasmic reticulum in the perinuclear region that is associated with abnormal glycogen deposition, and mislocalization of opsin immunoreactivity in rods. The rge/rge birds develop globe enlargement after the morphological and electroretinographic abnormalities. Globe enlargement in chicks can be induced by a number of different environmental factors. It is possible that abnormal signaling of photoreceptors to inner retinal cells could induce excessive ocular growth in the rge/rge birds. Many of the morphological changes such as retinal thinning seen in older rge/rge birds may be partly the result of the considerable globe enlargement that occurs later in the disease process. Molecular genetic studies to identify the causal gene mutation should help explain the morphological features of the rge/rge phenotype and clarify their association with vision loss and electroretinographic abnormalities.

Animals↗

Plasticity in adult cat visual cortex (area 17) following circumscribed monocular lesions of all retinal layers.

1. In eight adult cats intense, sharply circumscribed, monocular laser lesions were used to remove all cellular layers of the retina. The extents of the retinal lesions were subsequently confirmed with counts of alpha-ganglion cells in retinal whole mounts; in some cases these revealed radial segmental degeneration of ganglion cells distal to the lesion. 2. Two to 24 weeks later, area 17 (striate cortex; V1) was studied electrophysiologically in a standard anaesthetized, paralysed (artificially respired) preparation. Recording single- or multineurone activity revealed extensive topographical reorganization within the lesion projection zone (LPZ). 3. Thus, with stimulation of the lesioned eye, about 75 % of single neurones in the LPZ had 'ectopic' visual discharge fields which were displaced to normal retina in the immediate vicinity of the lesion. 4. The sizes of the ectopic discharge fields were not significantly different from the sizes of the normal discharge fields. Furthermore, binocular cells recorded from the LPZ, when stimulated via their ectopic receptive fields, exhibited orientation tuning and preferred stimulus velocities which were indistinguishable from those found when the cells were stimulated via the normal eye. 5. However, the responses to stimuli presented via ectopic discharge fields were generally weaker (lower peak discharge rates) than those to presentations via normal discharge fields, and were characterized by a lower-than-normal upper velocity limit. 6. Overall, the properties of the ectopic receptive fields indicate that cortical mechanisms rather than a retinal 'periphery' effect underlie the topographic reorganization of area 17 following monocular retinal lesions.

Animals↗

Optically induced plasticity of the cervico-ocular reflex in patients with bilateral absence of vestibular function.

The horizontal cervico-ocular reflex (COR) was examined in five labyrinthine-defictive subjects (LDS), during both passive oscillations of the head on the trunk (HTexam) and of the trunk under the earth-fixed head (THexam) at 0.1-0.5 Hz, peak angular displacement +/- 30 degrees. Subjects were tested in the dark, before and immediately after adaptation to binocular magnifying (x1.9) and reducing (x0.6) lenses. During long-term adaptation, the LDS were exposed to the normal environment for 5 h while wearing lenses. Short-term adaptation experiments (15-20 min) consisted of sustained ocular following of a small LED in an otherwise dark room and in full-room illumination. This LED was either stationary in space whilst the subjects moved their head actively, or fixed on the chair and rotating with the trunk during head-fixed stimulation. In all five patients, magnifying lenses increased COR gain (peak slow-phase eye velocity/peak stimulus velocity), whereas reducing lenses reduced the gain. Under HTexam the gain changes were greater, more consistent and the phases approximately compensatory to head displacement, whereas during THexam the gain decreased and phase increased at higher frequencies. COR adaptation was observed during foveal stimulation alone, but the effects were stronger with added background illumination. Results during an imaginary target task showed that the gain can be influenced strongly by mental set. Our findings indicate a highly modifiable COR in subjects with loss of vestibular function. Both peripheral and foveal retinal information contribute to the plastic changes in COR gain. Somatosensory cues from the trunk as well as cognitive/perceptual factors may be involved in the modification of the COR, by providing information about the relevance of eye movements, and contribute to the stabilisation of gaze in space.

Adult↗

Levels of dopamine and noradrenaline in the developing of retina--effect of light deprivation.

The effect of light deprivation on the levels of dopamine and noradrenaline was studied in the developing rat retina. These transmitters were estimated in three groups of rats: (i) cycling light reared; (ii) dark reared since birth; and (iii) dark reared since birth, but exposed to cycling light for 1 day prior to the estimation of catecholamines. Our results show that (1) there is a progressive decrease in the levels of dopamine and noradrenaline in the cycling light and dark reared rats during postnatal development; (2) dark rearing further reduces the content of dopamine and noradrenaline; and (3) restoration of physiological (light) stimulus in the dark-reared rats during the early postnatal period results in the recovery of noradrenaline to a greater extent than that of dopamine. This study demonstrates a progressive decrease in the plasticity of dopaminergic system during retinal development, while such a decrease is not apparent in the noradrenergic system.

Animals↗

Nucleus cryoinversion for extraction of highly complicated cataracts.

We describe a technique for cataract extraction in vitrectomized eyes that uses secured removal of the nucleus with no manipulation of the capsular bag. After a large scleral tunnel is prepared and a capsulorhexis created, a 20-gauge retinal cryoprobe enveloped in a plastic or a silicone sleeve is introduced into the anterior chamber. The cryoprobe engages the nucleus by a "freeze-grip" and rotates it 180 degrees so that the nucleus is elevated into the anterior chamber with no force applied to the capsule and the cryoprobe supporting it from below. The cryoprobe is replaced by a vectis under the nucleus and with the help of another instrument from above, the nucleus is removed. Aspiration of cortical material under low-pressure fluid maintenance of the anterior chamber completes removal of the cataract. An intraocular lens is then implanted in the ciliary sulcus for maximum capsule support.

Capsulorhexis↗