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At least 127 records · Page 7Linked to original sources
PubMed2001

Plastic response of the retrospleniocollicular connection after removal of retinal inputs in neonatal rats. An anterograde tracing study.

The effects of neonatal enucleation on the final adult pattern of retrospleniocollicular connection in the rat was studied using the anterograde tracer biotindextranamine 10,000 (BDA) iontophoretically injected in different anteroposterior locations of the retrosplenial cortex. Retrosplenial afferents are normally distributed in all collicular layers beneath the stratum griseum superficiale (SGS) throughout almost the entire rostrocaudal and lateromedial collicular axes. Neonatal enucleation caused an invasion of lower SGS by abundant retrosplenial afferents, whose distribution remained unaltered in intermediate and deep collicular layers. Axons entering the deafferented SGS showed variable morphologies and arborization patterns. Some of them ran lateromedially close to the SGS-stratum opticum (-SO) limit, giving rise to many collaterals which invaded the lower part of the SGS; whereas others formed narrow terminal arbors, mostly branching in the SO. In the intermediate layers, synaptic profiles were mainly found close to the borders of acetylcholinesterase (AChE) patches in both control and enucleated animals, indicating that neonatal enucleation does not alter the final pattern of retrospleniocollicular afferents to these collicular regions. The results presented here demonstrate that neonatal enucleation leads to the development of an aberrant projection from the retrosplenial cortex to the deafferented superficial layers of the superior colliculus. These results provide new information regarding the reorganization of connections subsequent to neonatal enucleation and suggest that, in enucleated animals, nonvisual multisensorial information could be relayed to central circuits which in intact animals belong to the visual system.

Animals↗
PubMed2006

Retinal functional development is sensitive to environmental enrichment: a role for BDNF.

Retina has long been considered less plastic than cortex or hippocampus, the very sites of experience-dependent plasticity. Now, we show that retinal development is responsive to the experience provided by an enriched environment (EE): the maturation of retinal acuity, which is a sensitive index of retinal circuitry development, is strongly accelerated in EE rats. This effect is present also in rats exposed to EE up to P10, that is before eye opening, suggesting that factors sufficient to trigger retinal acuity development are affected by EE during the first days of life. Brain derived neurotrophic factor (BDNF) is precociously expressed in the ganglion cell layer of EE with respect to non-EE rats and reduction of BDNF expression in EE animals counteracts EE effects on retinal acuity. Thus, EE controls the development of retinal circuitry, and this action depends on retinal BDNF expression.

Animals↗
PubMed1989

Evidence for the stability of positional markers in the goldfish tectum.

Positional markers in the tectum, which are thought to guide growing axons to their target sites, have been proposed to be induced by axons, to be only transiently associated with the tectal cells, and then lost after long-term denervation periods (Schmidt: J. Comp. Neurol. 177:279-300, '78). To further investigate this concept, retinal axons were induced to regenerate into ipsilateral tecta which had been deprived of their retinal afferents for shorter (0-4 months) and longer periods (4-8 months). The paths of HRP-labeled regenerating axons of known retinal origin were traced and used as an operational test to decide whether the axons might navigate under the influence of positional markers. Two different kinds of experiments were performed: 1. The axons from a subpopulation of all ganglion cells in the retina were labeled by applying a small crystal of HRP at defined retinal regions. Independent of the denervation period of the tectum, the labeled regenerating axons traveled in abnormal but nonrandom routes. In early regeneration stages, axons exhibited signs of exploratory growth. They extended branches equipped with growth cones and filopodia into various regions of the tectum. In late regeneration stages, the axons lost these branches, exhibited U-turns and bends, and ended in terminal arbors in the retinotopic target region. These findings suggest that the axons travel under the influence of tectal positional markers and that these markers are not transient. 2. Axons from a surgically created temporal hemiretina were labeled by application of HRP to the optic nerve to test whether the temporal axons might expand into the caudal tectum in long-term-denervated tecta. The HRP-labeled axons coursed over rostral and midtectal regions. Instead of invading the caudal tectum they bent and terminated in the rostral tectal half. These results add further support for the conclusion that the path of regenerating retinal axons is governed by long-lasting positional markers.

Animals↗
PubMed1976

Plasticity in the developing visual system: the effects of retinal lesions made in young rats.

The central visual pathways of the rat have been used as a model for investigating the significance of axonal interactions in mammalian neural development. Attention is restricted largely to the aberrant distribution of optic axons to the ipsilateral side of the brain and their distribution in the superior colliculus after early unilateral eye damage. The normal ipsilateral retinotectal pathway in pigmented rats appears as a series of patches located anteriorly and laterally in the stratum opticum, whereas in albino animals it is a small area lying anteromedially. In both, a few axons are often found at the extreme posterior border of the superior colliculus. After unilateral eye enucleation at birth, an aberrant ipsilateral pathway from the remaining eye arises at the optic chiasm. It originates from all parts of the retina and terminates in the ipsilateral superior colliculus in a topographic fashion such that the upper retina projects laterally and the lower retina, medially. The pathway is heaviest anteromedially (from lower temporal retina) and lightest posterolaterally (from upper nasal retina). There is always a heavy projection to the extreme posterior border of the superior colliculus. In only two animals of a large series was direct intertectal sprouting found. After partial retinal lesions, there is again an ipsilateral pathway from the unlesioned eye which fills the projection area of the lesion. As after total enucleation, the pathway arises from most of the ipsilateral retina, not just that region homotypic to the lesion site, being heaviest from the lower temporal and lightest (or deficient) from the upper retina. There is suggestion of ordering of the projection into the deafferented region in that the ipsilateral degeneration after lesions in the intact eye is compact but does not fill the gap in the crossed projection completely. There is also indication that some intact parts of the retina lesioned at birth may also project in an inappropriate retinotopic fashion to the deafferented region. The corticotectal pathway shows a normal map. Study of the ipsilateral retinotectal pathway indicates that the axons terminating at the extreme posterior border of the superior colliculus arise from the lower temporal retina. The results are interpreted as indicating that the aberrant uncrossed pathways after complete or local retinal lesions, compare very closely in most features. Both distribute to the deafferented area of the superior colliculus -- in one, this is the whole surface, while in the other it is a small area. The fact that in the latter case axons are ending in quite inappropriate parts of the tectal map, may be explained more simply in terms of interactions between adjacent axons in the optic pathway rather than by an hypothesis involving a change in the cell labels across the tectal map.

Age Factors↗
PubMed1989

Morphological and functional studies of rat tectal transplants.

Donor tectal tissue from fetal rats was transplanted to the tectal region of intact host newborn rats. Histological and ultrastructural characteristics of mature tectal grafts were examined with special emphasis placed on glial elements and the interface between transplant and host brain. Most transplants survived, proliferated, and differentiated to mature neurons and glial cells. Mature transplants were found to contain small and medium sized neurons which formed clusters along the transplant border. Neurites traversed the interface between transplant and host brain. There was an absence of phagocytosis, inflammatory reactions and chromatolytic neurons throughout the transplant. Classical staining techniques and GFAP immunoreactive stains revealed only mild focal astrogliosis confined mostly to the subpial and perivascular regions of the transplant-host interface. Ultrastructural examination of the transplant revealed numerous axodendritic synapses with aggregates of synaptic vesicles and well formed postsynaptic membranes. The absence of a leptomeningeal membrane at several points along the transplant-host interface may allow neurites from both sides to establish functional synaptic contacts. Single unit recording combined with anterograde WGA-HRP neuronal tract tracing was used to determine the presence and extent of host retinal innervation of tectal transplants.

Action Potentials↗
PubMed1992

Differentiation of retinal precursor cells born in vitro.

It is not known whether the differentiated fate of retinal precursor cells is determined before, during, or after terminal mitosis. Previous studies from this laboratory led to the hypothesis that retinal precursor cells remain plastic after final mitosis and will follow a photoreceptor "default pathway" unless induced to develop as neurons by intraretinal factors. This hypothesis predicts that isolated precursors undergoing terminal mitosis and differentiation in cell culture, in the absence of the retinal microenvironment, should become photoreceptors, regardless of embryonic age. To test this prediction precursor cells were dissociated from 5- to 8-day chick embryo retinas and grown as single cells in vitro. Bromodeoxyuridine (BRDU)- and [3H]thymidine-labeling techniques, coupled with serial photography of precursor development in culture, showed that at all donor ages some of the isolated cells divided one or more times and became postmitotic in vitro. Analysis of cell phenotype by phase-contrast microscopy, sequential photography, autoradiography, and immunocytochemistry showed that the majority of precursors from all donor ages differentiated as photoreceptors. These observations support a prediction derived from the "photoreceptor default" hypothesis.

Animals↗
PubMed2005

Retinal remodelling.

Retinal degenerative diseases that progress through loss of photoreceptors initiate a sequence of events that culminates in negative remodelling of the retina. Initially, photoreceptor loss ablates glutamatergic signalling to the neural retina and eliminates coordinate Ca++-coupled homeostatic signalling. Retinal neurons react to this loss of glutamatergic input through retinal rewiring and migration of neurons throughout the axis of the retina. All diseases that kill photoreceptors trigger retinal remodelling as the final common pathway and cell death is a common feature. Retinal remodelling resembles CNS pathologic remodelling and constitutes a major challenge to all rescue strategies.

Amacrine Cells↗
PubMed2003

Retinal remodeling triggered by photoreceptor degenerations.

Many photoreceptor degenerations initially affect rods, secondarily leading to cone death. It has long been assumed that the surviving neural retina is largely resistant to this sensory deafferentation. New evidence from fast retinal degenerations reveals that subtle plasticities in neuronal form and connectivity emerge early in disease. By screening mature natural, transgenic, and knockout retinal degeneration models with computational molecular phenotyping, we have found an extended late phase of negative remodeling that radically changes retinal structure. Three major transformations emerge: 1) Müller cell hypertrophy and elaboration of a distal glial seal between retina and the choroid/retinal pigmented epithelium; 2) apparent neuronal migration along glial surfaces to ectopic sites; and 3) rewiring through evolution of complex neurite fascicles, new synaptic foci in the remnant inner nuclear layer, and new connections throughout the retina. Although some neurons die, survivors express molecular signatures characteristic of normal bipolar, amacrine, and ganglion cells. Remodeling in human and rodent retinas is independent of the initial molecular targets of retinal degenerations, including defects in the retinal pigmented epithelium, rhodopsin, or downstream phototransduction elements. Although remodeling may constrain therapeutic intervals for molecular, cellular, or bionic rescue, it suggests that the neural retina may be more plastic than previously believed.

Aging↗
PubMed2002

Plastic reaction of the rat visual corticocollicular connection after contralateral retinal deafferentiation at the neonatal or adult stage: axonal growth versus reactive synaptogenesis.

The effects of neonatal or adult enucleation on the final adult pattern of the rat visual corticocollicular (C-Co) connection were studied using the anterograde tracer biotinylated dextranamine 10,000 (BDA) iontophoretically injected in the primary visual cortex. In control animals, column-shaped terminal fields limited to a small portion of the collicular surface were observed. Synaptic boutons were present in all superficial strata of the superior colliculus (SC), with the highest density in the ventral part of the stratum griseum superficiale (SGS). Neonatal enucleation caused a considerable expansion of the contralateral visual C-Co terminal fields, which occupied almost the entire collicular surface, suggesting that axonal sprouting had occurred. In addition, terminal boutons tended to localize more dorsally in these cases compared with controls. Following enucleation in adult animals, no changes were observed with respect to the extension of the terminal fields, although a plastic reaction leading to an increase in the bouton density in the stratum zonale (SZ) and upper SGS was found, reflecting a process of reactive synaptogenesis at these levels. These results show that both neonatal and adult visual C-Co fibers react in response to retinal ablation, although this reaction shows distinct characteristics. Molecular factors, such as growth-associated cytoskeletal proteins operating in the cortical origin, and extracellular matrix components and myelin-associated axonal growth inhibitors acting on the collicular target very likely account for these differences.

Age Factors↗
PubMed1990

Ultrastructural and immunocytochemical changes in retinal pigment epithelium, retinal glia, and fibroblasts in vitreous culture.

Retinal pigment epithelial (RPE) cells, retinal glial, and fibroblasts, three cell types believed to play a role in the pathogenesis of epiretinal membrane formation, were maintained in vitreous culture to determine the influence of vitreous on their ultrastructure and expression of cytokeratin, glial fibrillary acidic protein (GFAP), vimentin, and glutamine synthetase (GS). Using a highly sensitive, preembedding technique for the immunolocalization of these antigens at the ultrastructural level, most RPE cells were found to lose cytokeratin and vimentin within 1 day after seeding on irradiated vitreous. The percentage of keratin-positive cells then increased with time in culture. If the vitreous was placed on RPE cells cultured in monolayer instead of placing the cells on the vitreous, keratin and vimentin were expressed these intermediate filament proteins diminished with time. Glutamine synthetase was found in RPE cells grown in monolayer with or without a vitreous overlay, but not in RPE cells grown on the surface of vitreous. Retinal glial grown on vitreous showed a time-dependent decrease in the number of cells expressing GFAP and a corresponding increase in cells expressing vimentin or GS. Some fibroblasts in vitreous culture expressed vimentin but not the other antigens evaluated. A substantial number of cells in each culture did not stain positively for cytokeratin, GFAP, vimentin, or GS. All three cell types showed phenotypic diversity at the ultrastructural level with each cell type being capable of assuming the same morphologic appearance under certain conditions. These results demonstrate the phenotypic plasticity of RPE cells, retinal glia, and fibroblasts when grown in contact with vitreous and provide further evidence that neither ultrastructure, intermediate filament protein expression, nor the presence of GS is sufficient to determine the cell type of origin of cells in epiretinal membranes.

Animals↗
PubMed2006

Visual hallucinations during visual recovery after central retinal artery occlusion.

BACKGROUND: Charles Bonnet syndrome is characterized by complex, formed visual hallucinations that occur in patients without psychiatric disorders. To the best of our knowledge, it has not been described following central retinal artery occlusion. OBJECTIVE: To describe 2 patients who experienced formed visual hallucinations characteristic of Charles Bonnet syndrome after sudden, severe visual loss precipitated by central retinal artery occlusion. PATIENTS: Two patients, aged 77 and 63 years respectively, experienced sudden deterioration of vision following central retinal artery occlusion. Formed visual hallucinations occurred in patient 1 six days later and in patient 2 two days later. RESULTS: The hallucinations appeared both within and at the borders of the patients' residual intact visual fields. They occurred during periods when the patients experienced partial visual recovery associated with enlargement of their visual fields. The visual recovery and hallucinations both ceased at the same time. CONCLUSIONS: We propose that the hallucinations are likely the result of deafferentation and their occurrence during visual recovery suggests that they are a correlate of visual system plasticity.

Aged↗
PubMed1996

Fine structure of the pecten oculi in the Australian galah (Eolophus roseicapillus) (Aves).

The pecten oculi of the Australian galah (Eolophus roseicapillus) has been examined by both light and electron microscopy. In this species the pecten is large relative to the size of the eye and is of the pleated type. It consists of 20-25 accordion folds that are joined apically by a bridge of tissue which holds the pecten in a fan-like shape widest at its base. Within each fold are many melanocytes, numerous capillaries as well as larger supply and drainage vessels. The capillaries are extremely specialized for transport functions and display extensive microfolds on both their luminal (inner) and abluminal (outer) borders. Except for the nuclear region which also contains most of the organelles, the endothelial cell bodies are extremely thin. These capillaries are surrounded by thick fibrillar basal laminae which are felt to be structurally important. Pericytes are a common feature within the basal lamina of capillaries. The numerous pleomorphic melanocytes which more or less surround the capillaries are also presumed to be important in structural support of the pecten. The pecten represents a supplementary retinal circulation and is comparable to the falciform process of some teleosts, the conus papillaris of reptiles, the supraretinal vessels of amphibians and some teleosts and the intraretinal vessels of mammals, all of which are felt to be alternative methods of bringing nutrients to the inner retina.

Adaptation, Ocular↗
PubMed2004

Visual experience and maturation of retinal synaptic pathways.

The retinal synaptic network continues its maturational refinement after eye opening in mammals. This synaptic refinement is reflected in changes of retinal neuron synaptic activity and connectivity. In mature retina, the dendrites of retinal ganglion cells (RGCs) in the inner plexiform layer (IPL) of retina are separated into ON or OFF sublamina. At early developmental stage, however, the dendrites of most RGCs are ramified throughout the IPL. Recently we found that the postnatal maturational processes converting bistratified ON-OFF responsive RGCs to monostratified ON and OFF responsive RGCs depend upon visual stimulation after eye opening.

Aging↗
PubMed1984

Retinal-image degradation produces ocular enlargement in chicks.

Two groups of 3-day-old broiler chicks were fitted over the right eye with plastic goggles that degraded the retinal image by producing spherical aberration, reduction of contrast, and blurring of edges. In one group of chicks, the goggles were hemispheric and affected the entire visual field. In the second group, the goggles only affected the frontal visual field. In both groups, the left eye was used as a control. A third group of chicks served as an untreated control group. After 3 weeks, the chicks were killed, the eyes removed, hemisected, and measured in the axial and equatorial planes. Because the avian eye is flattened in the equatorial plane, both sets of measurements are necessary in order to represent changes in its size and shape. The axial length of a laterally located avian eye is related to distance vision. The equatorial length is related to vision in the frontal field, which is used for near vision. For each group of chicks, the difference between the right eye and the left eye was compared. The treated eyes of the full- goggle group were significantly larger than their untreated eyes in both the axial and equatorial dimensions. The treated eyes of the frontal- goggle group differed only in the equatorial dimension. These results suggest that the increased equatorial length found after retinal-image degradation may serve as an animal model of myopia.

Animals↗
PubMed1989

Pathfinding and target selection of goldfish retinal axons regenerating under TTX-induced impulse blockade.

To define the extent to which impulse blockade interferes with the morphological changes of regenerating retinal axons during their growth through the tectum, axons were deprived of activity by repeated intraocular injections of TTX. At intervals between 24 and 189 days after optic nerve section (ONS), a defined group of TTX-silenced axons and of axons with normal activity (controls) were labeled by applications of HRP to the ventro- or dorsotemporal retina. The trajectories of these labeled axons were traced in DAB processed tectal wholemounts. As in controls, TTX-blocked axons went through a phase of exploratory growth at early regeneration stages (24 to 80 days after ONS). Coursing in abnormal routes, the axons initially distributed their growing endings widely over the tectum. Axons with and without activity extended side branches with growth cones and filopodia over all regions of the tectum. These ramifications were of similar dimensions for the TTX-blocked and control axons. Despite abnormal routes and branching over inappropriate territories, axons showed a preference for the rostral tectum. At late regeneration stages (120-189 days after ONS), axons had lost their side branches and their growth cones. Their preterminal segments exhibited striking bends, suggesting that they had undergone course corrections to achieve access to the retinotopic target. Axonal processes had disappeared from the caudal tectum, and the preferential accumulation of axons over the rostral tectum had increased. The majority of the TTX-blocked and control axons ended in terminal arbors at retinotopic regions. The labeled arbors of the TTX-group were no larger than those of the control group. The arbors of each group lay close together in a continuous cluster in the TTX-group as well as in two-thirds of the control group. In the other one-third of the control group, however, terminal arbors were aggregated into separate patches. The clusters of the TTX-blocked axons covered between 2.2 and 3.9% (mean 2.95%) of the tectal surface and the clusters and/or patches of active axons between 1.9 and 3.4% (mean 2.7%). Thus the terminal arbor clusters of the TTX-silenced axons were not significantly larger than those of the active axons. These data show that retinal ganglion cell impulse activity is required for neither the extension of side branches in the early exploratory phase of regeneration nor for the withdrawal of these branches nor for the establishment of target-directed routes and the deployment of normal-size terminal arbors at retinotopic loci.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2003

Topographic plasticity in primary visual cortex is mediated by local corticocortical connections.

The placement of monocular laser lesions in the adult cat retina produces a lesion projection zone (LPZ) in primary visual cortex (V1) in which the majority of neurons have a normally located receptive field (RF) for stimulation of the intact eye and an ectopically located RF (displaced to intact retina at the edge of the lesion) for stimulation of the lesioned eye. Animals that had such lesions for 14-85 d were studied under halothane and nitrous oxide anesthesia with conventional neurophysiological recording techniques and stimulation of moving light bars. Previous work suggested that a candidate source of input, which could account for the development of the ectopic RFs, was long-range horizontal connections within V1. The critical contribution of such input was examined by placing a pipette containing the neurotoxin kainic acid at a site in the normal V1 visual representation that overlapped with the ectopic RF recorded at a site within the LPZ. Continuation of well defined responses to stimulation of the intact eye served as a control against direct effects of the kainic acid at the LPZ recording site. In six of seven cases examined, kainic acid deactivation of neurons at the injection site blocked responsiveness to lesioned-eye stimulation at the ectopic RF for the LPZ recording site. We therefore conclude that long-range horizontal projections contribute to the dominant input underlying the capacity for retinal lesion-induced plasticity in V1.

Animals↗
PubMed1994

Modulation of gap-junction channel gating at zebrafish retinal electrical synapses.

1. Transmission at electrical synapses is modulated by a variety of physiological signals, and this modulation is a potentially general mechanism for regulating signal integration in neural circuits and networks. In the outer plexiform layer of the retina, modulation of horizontal-cell electrical coupling by dopamine alters the extent of spatial integration in the horizontal-cell network. By analyzing the activity of individual gap-junction channels in low-conductance electrical synapses of zebrafish retinal horizontal cells, we have defined the properties of these synaptic ion channels and characterized the functional changes in them during modulation of horizontal-cell electrical synapses. 2. Zebrafish horizontal-cell gap-junction channels have a unitary conductance of 50-60 pS and exhibit open times of several tens of milliseconds. The kinetic process of channel closure is best described by the sum of two rate constants. 3. Dopamine, and its agonist, (+/-)-6,7-dihydroxy-2-amino-tetralin (ADTN), modulates electrical synaptic transmission between horizontal cells predominantly by affecting channel-gating kinetics. These agents reduced the open probability of gap-junction channels two- to threefold by reducing both the duration and frequency of channel openings. Both time constants for channel open duration were reduced, whereas the duration of shut periods was increased. Similar changes in open-time kinetics were observed in power spectra of higher conductance gap junctions. 4. These results provide a description of rapid electrical synaptic modulation at the single channel level. The description should be useful in understanding the mechanisms of plasticity at these synapses throughout the vertebrate central nervous system.

Animals↗