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Results for “retinal plasticity”

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At least 37 records · Page 2Linked to original sources
PubMed1995

Morphological plasticity of axotomized retinal ganglion cells following intravitreal transplantation of a peripheral nerve segment.

During normal development of retinal ganglion cells when the axons are growing, transient dendritic spines have been observed. Similar dendritic spine-like processes are also exhibited by retinal ganglion cells undergoing axonal regeneration into a peripheral nerve grafted to the damaged optic axons. Here we show, using the intracellular injection of Lucifer Yellow, that when a segment of peripheral nerve is transplanted to the vitreous body, a procedure which induces ectopic sprouting of axon-like processes from the cell bodies and dendrites of some retinal ganglion cells, similar spine-like processes appear on the dendrites of cells with ectopic sprouts. Quantitative analysis indicated that there were significant changes with posttransplantation survival time in the distributions of spine-like processes and axon-like processes on these sprouting retinal ganglion cells following the intravitreal transplantation of a piece of peripheral nerve. The remodelling of the spine-like processes and axon-like processes correlated with one another suggesting that plastic changes can occur in certain dendritic subcompartments independent of the growth activity of the other dendritic subcompartments.

Animals↗
PubMed1990

Substance P and enkephalins in the superficial layers of the rat superior colliculus: differential plastic effects of retinal deafferentation.

In this work we studied the effects of unilateral eye enucleation on the contents and distribution of leu-enkephalin-, met-enkephalin-arg6-gly7-leu8-, and substance-P-like immunoreactivities (L-ENK-I, ENK-8-I, and SP-I, respectively) in the superficial layers of the rat superior colliculus (SC) by means of the unlabelled antibody peroxidase-antiperoxidase method. In the normal rat only a few L-ENK-I neurons appear dispersed in the stratum griseum superficiale. No immunostained somata appear in the stratum opticum. The most striking effect of unilateral enucleation was the dramatic appearance of a laminarly distributed population of L-ENK-I and/or ENK-8-I neurons in the dorsal stratum opticum of the SC contralateral to the enucleated side. This population of immunoreactive cells was observed with all the survival times examined in the present study (3, 7, 15, and 30 days) and was always accompanied by an increase in the immunostaining of L-ENK-I and/or ENK-8-I fibers in the contralateral stratum griseum superficiale. Enucleation also produced a decrease in the immunostaining of SP-I dendrites that only became obvious 15 days after enucleation. However, the number of SP-I somata or terminal-like immunoreactive structures showed no detectable changes. These results show that retinal deafferentation of the superficial layers of the rat SC has different effects on some immunohistochemically distinguishable neuronal subgroups in the SC, suggesting different functional or trophic relationships of the retinal input to these groups of neurons.

Afferent Pathways↗
PubMed1994

Plasticity in mesencephalic and retinal polarity formation in avian embryos.

Polarity and its plasticity in the avian mesencephalon and the retina are reviewed. Rostrocaudal polarity of the tectum (dorsal mesencephalon) is revealed by the gradient of engrailed gene expression, by its cytoarchitecture, and by positional specification of tectal cells which retinal fibers read to find their targets. In the ventral mesencephalon, the polarity is revealed by directional growth of tectofugal axons. To examine the plasticity in rostrocaudal polarity, rostrocaudal orientation of the mesencephalon was surgically reversed on E2. Rostrocaudal polarity of the reversed mesencephalon was all adjusted to the host pattern. This suggests that the mesencephalic polarity is not fixed on E2 and is established under environmental influences. Retinal polarity is revealed by the distribution of certain molecules, by retinal structures, and by the retinotectal projection pattern. Retinal structures and retinotectal projection pattern were kept as in the original if retinal primordium was rotated or partially excised after stages 12-14 of Hamburger and Hamilton. The location of an optic fissure and the retinal fiber pattern were adjusted to those of normal eyes when the rotation was performed before stage 12, therefore the retinal polarity was supposed to be plastic before stage 12 and to be fixed around the stages 12-14 under environmental influences.

Animals↗
PubMed2001

Cortical plasticity revealed by circumscribed retinal lesions or artificial scotomas.

We review the work of others in which the effects of circumscribed, topographically corresponding binocular retinal lesions on the topographic organization of the visual cortex revealed that there is a substantial degree of topographical plasticity in the primary visual cortices of adult cats and macaque monkeys. Despite the evidence indicating that the reorganization of the topographic map in primary visual cortices of adult cats and macaques related to the input from one eye could be suppressed for a long time by inputs related to the other eye, we observed a substantial degree of topographical plasticity in the primary visual cortices of adult cats in which we have made circumscribed monocular retinal lesions. Overall, in both binocularly and monocularly lesioned adult animals, most cells recorded in the cortical projection zone of the retinal lesion (LPZ), several hours, several weeks or several months after placement of the lesions exhibited 'ectopic' excitatory visual receptive fields (RFs) which were displaced to the normal retina in the immediate vicinity of the lesion. The presence of ectopic RFs in cells recorded in the cortical LPZ, combined with the presence of normal cortical representation of the part of the retina in the vicinity of the lesion, indicate a clear expansion of the cortical representation of the part of the retina surrounding the lesion. When stimulated via the ectopic RFs, cortical cells exhibited normal orientation tuning and in the case of animals with monocular lesions, the orientation tuning of binocular cells when stimulated via ectopic RFs appeared to be very similar to that when the cells were stimulated via the RFs in the normal, unlesioned eye. In both binocularly and monocularly lesioned animals, the responses evoked by optimal visual stimuli from the ectopic RFs were substantially weaker than those evoked from their normal counterparts. Similarly, upper velocity limits were significantly lower when visual stimuli were presented via the ectopic RFs. In contrast to cats in which the retinal lesions were made in adulthood, in cats lesioned monocularly in adolescence (8-11 weeks postnatal), both the peak discharge rates and upper velocity limits of responses to photic stimuli presented via the ectopic RFs were very similar to those to stimuli presented via the normal eye. The intracortical mechanism(s) underlying the long-term cortical plasticity revealed by retinal lesions are likely to be closely linked to the mechanism(s) underlying the short-term reversible enlargement of cortical receptive fields observed with artificial scotomas. Furthermore, a similar putative intracortical mechanism(s) appears to underlie psychophysical phenomena observed in studies of retinal scotomas in humans. Overall, the research reviewed here strongly challenges the view that receptive fields of neurons in mammalian visual cortices are 'hard-wired'.

Animals↗
PubMed1992

Protective effects of flunarizine on ischemic injury in the rat retina.

Intracellular calcium overload has been implicated to be a major factor in triggering cell death after ischemic neuronal injury. We investigated the effects of flunarizine hydrochloride, a calcium-overload blocker, on pressure-induced retinal ischemia in a rat model. Retinal ischemia was induced in intraocular pressure to 110 mm Hg for 45 minutes. Two regimens of treatment with flunarizine were examined: (1) prophylactic treatment, in which flunarizine was administered before ischemia and in the early phase of reperfusion; and (2) postischemic treatment, in which flunarizine was administered only in the early phase of reperfusion. Injury was evaluated morphologically and morphometrically by measuring the thickness of the inner retinal layers on plastic-embedded retinal sections and by counting the retinal ganglion cells on retinal flat preparations. By morphologic and morphometric criteria, a significant but partial protection of the inner retinal layers was noted in the groups given either regimen. This protective effect of flunarizine suggests that elevated intracellular calcium concentration may play an important role in ischemic retinal injury.

Animals↗
PubMed1996

Ca(2+)-dependency of spinule plasticity at dendrites of retinal horizontal cells and its possible implication for the functional role of spinules.

Calcium is involved in many aspects of synaptic plasticity and we have analyzed its involvement in spinule dynamics at retinal horizontal cell dendrites. We show here that in particular the retraction of spinules is a Ca(2+)-dependent process. Inhibiting calmodulin or CaMKII, blocked the retraction that was also impaired in low calcium Ringer. Changes of the cytosolic Ca(2+)-concentration through depletion of internal Ca(2+)-stores were without effect. This suggested that Ca(2+)-influx during dark adaption and subsequent activation of CaMKII is an important step for spinule retraction. Voltage dependent Ca(2+)-channels were not responsible for the Ca(2+)-influx, rather Ca2+ leaking through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate-gated channels. This suggested a close local link between AMPA/kainate receptors and CaMKII indicating a possible postsynaptic function of spinules. The distribution of bound, omega-shaped vesicles within the cone pedicles and its dependence on artificial depolarization further supported the idea of a postsynaptic function of spinules.

Adaptation, Ocular↗
PubMed1993

Rapid plastic response following early retinal lesions in rats.

Following an early retinal lesion, aberrant uncrossed projections from the opposite, undamaged, retina form in the target visual nuclei. The present study has examined the development of such aberrant projections by making retinal lesions in newborn rat pups, and then examining the nature of the uncrossed retinocollicular projection at different ages following the lesion. Intravitreal injections of horseradish peroxidase were made into the intact eye, and the uncrossed projection was subsequently revealed histochemically. A mature aberrant projection forms as early as postnatal day 9. On postnatal days 5 and 2, aberrant projections are discernable amongst the exuberant uncrossed terminals of normal developing rats, although the former have not matured to form the dense terminal fields characteristic of older projections. Aberrant projections were also detectable as early as 12 h following the lesion, revealed as a relative increase in the density of uncrossed label. These results indicate that lesion-induced plastic responses by intact retinal arbors are initiated shortly after the insult, and they caution the use of retinal lesions in studies of normal retinotopic connectivity during development.

Animals↗
PubMed1990

Development of abnormal lamination and binocular segregation of retinal afferents onto the rat superior colliculus.

Unilateral optic tract lesions made in newborn rats produce abnormal retinotectal pathways on the opposite side. The present investigation was designed to study the development of the abnormal retinal projections in the superior colliculus using anatomical tracing methods. The aberrant uncrossed retinotectal pathway develops within the first postnatal week. In spite of this, the retraction of the crossed projection, which indicates binocular segregation, is of late onset. This indicates that the induced segregation of retinal inputs is not dependent on regressive events such as ganglion cell death and terminal field retraction. These data and the results of lid-suture experiments are consistent with a role for spontaneous retinal activity in the regulation of the plasticity of retinal projections to the rat superior colliculus.

Animals↗
PubMed2005

Endothelial survival factors and spatial completion, but not pericyte coverage of retinal capillaries determine vessel plasticity.

Pericyte loss and capillary regression are characteristic for incipient diabetic retinopathy. Pericyte recruitment is involved in vessel maturation, and ligand-receptor systems contributing to pericyte recruitment are survival factors for endothelial cells in pericyte-free in vitro systems. We studied pericyte recruitment in relation to the susceptibility toward hyperoxia-induced vascular remodeling using the pericyte reporter X-LacZ mouse and the mouse model of retinopathy of prematurity (ROP). Pericytes were found in close proximity to vessels, both during formation of the superficial and the deep capillary layers. When exposure of mice to the ROP was delayed by 24 h, i.e., after the deep retinal layer had formed [at postnatal (p) day 8], preretinal neovascularizations were substantially diminished at p18. Mice with a delayed ROP exposure had 50% reduced avascular zones. Formation of the deep capillary layers at p8 was associated with a combined up-regulation of angiopoietin-1 and PDGF-B, while VEGF was almost unchanged during the transition from a susceptible to a resistant capillary network. Inhibition of Tie-2 function either by soluble Tie-2 or by a sulindac analog, an inhibitor of Tie-2 phosphorylation, resensitized retinal vessels to neovascularizations due to a reduction of the deep capillary network. Inhibition of Tie-2 function had no effect on pericyte recruitment. Our data indicate that the final maturation of the retinal vasculature and its resistance to regressive signals such as hyperoxia depend on the completion of the multilayer structure, in particular the deep capillary layers, and are independent of the coverage by pericytes.

Angiopoietin-1↗