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R C Van Sluyters

Publications and source records attributed to R C Van Sluyters.

At least 19 recordsLinked to original sources

Distribution of visual callosal neurons in normal and strabismic cats.

It has been suggested that synchronous activation of cortical loci in the two cerebral hemispheres during development leads to the stabilization of juvenile callosal connections in some areas of the visual cortex. One way in which loci in opposite hemispheres can be synchronously activated is if they receive signals generated by the same stimulus viewed through different eyes. These ideas lead to the prediction that shifts in the cortical representation of the visual field caused by misalignment of the visual axes (strabismus) should change the width of the callosal zone in the striate cortex. We tested this prediction by using quantitative techniques to compare the tangential distribution of callosal neurons in the striate cortex of strabismic cats to that in normally reared cats. Animals were rendered strabismic surgically at 8-10 days of age and were allowed to survive a minimum of 18 weeks, at which time multiple intracortical injections of the tracer horseradish peroxidase (HRP) were used to reveal the distribution of callosally projecting cells in the contralateral striate cortex. HRP-labeled cells were counted in coronal sections, and data from four animals with divergent strabismus (exotropia) and four with convergent strabismus (esotropia) were compared to those from four normally reared animals. Although our data from strabismic cats do not differ markedly from those reported previously, we find that the distribution of callosal cells in the striate cortex of these cats does not differ significantly from that in our normally reared control cats. These results do not bear out the prediction that surgically shifting the visual axes leads to stabilization of juvenile callosal axons in anomalous places within the striate cortex.

Animals↗

Overall pattern of callosal connections in visual cortex of normal and enucleated cats.

The effect of neonatal bilateral enucleation on the overall distribution of callosal connections in striate and extrastriate visual cortex of the cat was studied using tangential sections from the physically unfolded and flattened cortex. Callosal neurons were labeled by administering the anatomical tracer horseradish peroxidase directly to the transected corpus callosum. The pattern of callosal connections in binocularly enucleated cats showed both consistent differences and consistent similarities with the pattern in normal cats. In agreement with previous studies, it was found that callosal labeling at the 17/18 border of enucleated cats was considerably sparser than in normal cats. Moreover, we found that the strip containing the majority of labeled cells at the 17/18 border was narrower than in normal cats. In both normal and enucleated cats, scattered cells were distributed on either side of the 17/18 callosal strip, well into areas 17 and 18. In much of extrastriate cortex, the pattern of callosal connectivity in enucleated cats looked surprisingly normal. Details of the callosal pattern that were consistently found in normal cats could also be recognized in binocularly enucleated cats, such as two to four bridges of labeling spanning areas 18 and 19. Also, four zones that were free of callosal connectivity in area 7, on the banks of the suprasylvian sulcus, and in the posterior suprasylvian sulcus were found in both normal and enucleated cats. Finally, as in normal cats, dense cell labeling occurred on the crown of the suprasylvian gyrus at its posterior end, from which it extended laterally across both banks of the suprasylvian sulcus and into the fundus of this sulcus. The results of this study suggest that, although the stabilization of callosal connections at the 17/18 border region appears to depend on visual input, this input plays a less prominent role in the stabilization of callosal connections in extrastriate visual cortex.

Animals↗

Comparison of the patterns of callosal connections in lateral parietal cortex of the rat, mouse and hamster.

In a recent study of the second somatosensory area (SmII) in the rat it was reported that the somatotopic map in the cortex lateral to the primary somatosensory area (SmI) is closely related to local features of the callosal pattern. The existence of this relationship suggests that knowledge of the overall pattern of callosal connections in the cortex lateral to SmI may facilitate the description of the somatotopic organization of lateral parietal cortex in other rodents. We tested this suggestion by comparing the callosal patterns in lateral parietal cortex in the rat, mouse and hamster. Our finding that the callosal pattern in the mouse closely resembles that in the rat supports the idea that the callosal pattern reflects the underlying somatotopy because the maps of SmII described previously in the mouse and rat are very similar to each other. In addition, on the basis of our observation that the callosal pattern in the hamster is very similar to that in the rat and mouse, we predict that these three rodent species share a common somatotopic plan in lateral parietal cortex.

Animals↗

Cytochrome-oxidase blobs in cat primary visual cortex.

Cytochrome-oxidase blobs are central to two of the most influential ideas in contemporary visual neuroscience--cortical modularity and parallel processing pathways. In particular, the regular 2D array of cytochrome-oxidase-rich blobs in primate visual cortex is arguably the most compelling evidence for cortical modularity and has been hypothesized to mark a separate processing stream through the visual cortex. Although previously a variety of mammals have been studied, blobs have only been demonstrated in the visual cortex of primates, which has led to the conclusion that blobs represent a primate-specific feature of visual cortical organization. Here we demonstrate the presence of cytochrome-oxidase blobs in a nonprimate species. Throughout the full tangential extent of layers II-III in cat visual cortex the cytochrome-oxidase staining pattern is distinctly patchy, with the darkly stained blobs forming a regular 2D array. In addition, the blobs in cat visual cortex are functionally related to the underlying ocular dominance columns. The presence of cytochrome-oxidase blobs in the cat clearly demonstrates that they no longer can be considered a primate-specific feature of visual cortical organization.

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Effect of monocular blockade of retinal activity on the development of visual callosal connections in the rat.

It has been previously reported that neonatal monocular enucleation in rats and hamsters induces the development of an anomalous band of callosal connections in the middle of area 17 (primary visual cortex) in the hemisphere ipsilateral to the remaining eye. In order to determine whether this effect is due to elimination of retinal activity in one eye, we used the anatomical tracer horseradish peroxidase (HRP) to study the pattern of visual callosal connections in rats in which retinal activity had been blocked by intraocular injections of tetrodotoxin during the first two weeks of life. We found that the callosal pattern in the hemisphere ipsilateral to the eye not treated with tetrodotoxin was not distinguishable from the pattern present in normal rats. In particular, we did not observe the anomalous extra band of callosal connections that occurs in area 17 in the hemisphere ipsilateral to the remaining eye in monocularly enucleated rats. These results indicate that blockade of retinal activity in one eye is not sufficient to cause the marked changes in the pattern of visual callosal connections that are induced by neonatal monocular enucleation.

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A computational model for the overall pattern of ocular dominance.

In layer IV of the primary visual cortex, in both the macaque monkey and the cat, geniculocortical terminals representing the two eyes are segregated into alternating zones known as ocular dominance bands. Viewed tangentially, in the monkey these bands take the form of a series of branching parallel stripes that run roughly perpendicular to the border of striate cortex. In the cat, the overall ocular dominance pattern consists of irregularly branching, beaded bands that exhibit no predominant orientation. If the striking differences in the appearance of these two patterns reflect important differences in the basic rules governing cortical ocular dominance, then this poses a problem for attempts to formulate general principles of visual cortical organization. However, it has been suggested that the differences in the appearance of the ocular dominance patterns in these two species could result simply from known differences in the boundary conditions of their geniculocortical pathways. This article describes the formulation and testing of a single computational model that accurately predicts the quite dissimilar ocular dominance patterns in cats and monkeys. This model also generalizes to predict the different ocular dominance patterns observed in young and old three-eyed frogs, supporting the notion that the overall pattern of ocular dominance is governed by a common set of rules. The significance of these results is discussed in terms of previous models, which have focused largely on local processes underlying the development of ocular dominance segregation. Although the present model is not a developmental one, it does shed some light on potential mechanisms for establishing retinotopy in striate cortex and on possible developmental relationships between the geniculostriate pathway and intrinsic modularity of the striate cortex.

Animals↗

Strabismus does not prevent recovery from monocular deprivation: a challenge for simple Hebbian models of synaptic modification.

It has been suggested that development of central connections in the mammalian visual system is governed by a simple Hebbian rule of synaptic modifiability. Under such a rule, simultaneity of presynaptic and postsynaptic action potentials is a prerequisite for enhanced synaptic efficacy. The present paper reports the results of a study designed to test whether this hypothesis is applicable to the development of the thalamo-cortical visual pathway. In four-week-old kittens, exposure to a 2-d period of monocular deprivation was used to render the vast majority of cortical cells capable of being activated only by the nondeprived eye. During a subsequent 3-5 month recovery period, both eyes were open but surgically misaligned. This combination of conditions was chosen so that during the recovery period presynaptic activity originating from the initially deprived eye would be decorrelated from postsynaptic action potentials in cortical neurons. If synaptic modification is regulated by a simple Hebbian mechanism, then in this situation the deprived eye should be unable to recover control of cortical cells. In fact, the present results indicate that during the recovery period the proportion of cortical neurons dominated by the deprived eye rose to a level equal to that of the nondeprived eye--a result contrary to that predicted by a simple Hebbian rule of development. Histological analysis indicated that a similar level of recovery was present both within and outside of cortical layer IV, the main thalamo-recipient layer. As expected, the induced strabismus resulted in a failure of cortical binocularity to recover in these kittens. Although these results argue against a simple Hebbian mechanism of development, they are compatible with the hypothesis that synaptic modifiability is dependent upon correlations between presynaptic activity and local, subthreshold, postsynaptic changes. This alternative hypothesis has the advantage of allowing modification of local synaptic circuits within the dendritic arbors of a single neuron.

Action Potentials↗

Topography of interhemispheric connections in neocortex of mice with congenital deficiencies of the callosal commissure.

Normally, axons within the corpus callosum are ordered according to the cortical regions from which they originate, and callosal cells and terminations form elaborate cortical patterns related to the underlying topographic representations of the sensory periphery. About 30% of mice of the BALB/c strain show congenital deficiencies of the callosal commissure which range from total absence of the corpus callosum to a moderate reduction in the size of this commissure. In the light of current theories about the origin of these callosal deficiencies, it seems likely that fibers crossing the midplane in mutant mice have to circumvent local disturbances along their migration path. Since these disturbances in fiber trajectory may, in turn, alter the overall pattern of callosal projections, we set out to investigate whether the distribution of callosal connections in mice with marked deficiencies of the corpus callosum is as ordered as in normal mice. In groups of normal and mutant mice, we used multiple injections of horseradish peroxidase to reveal the overall distribution of callosal connections and restricted injections of horseradish peroxidase conjugated with wheat germ agglutinin to reveal finer aspects of the organization of the callosal pathway in these animals. Our results show that the number of labeled cells is reduced in mice with a small corpus callosum and that no labeled cells are present in the neocortex of acallosal mice. Furthermore, the topographic distribution of fibers within the corpus callosum of mutant mice can be significantly less ordered than in normal mice. However, even in mice with extreme deficiencies of the corpus callosum, callosal fibers originate from and terminate in all major areas of the cortex, and, within these areas, callosal cells and terminations are distributed according to the normal plan. The laminar distribution of callosal cells also appears normal in these mice. These findings indicate that gross developmental anomalies of the corpus callosum do not prevent normal specification of the callosal pattern during development. Within the context of current theories about the origin of congenital callosal deficiencies, our findings suggest that callosal fibers are able to establish appropriate contralateral connections in spite of alterations of their migration route. They also suggest that fiber topography within the corpus callosum does not play an important role in guiding migrating axons to their correct contralateral targets. Finally, our failure to find labeled fibers within the anterior commissure indicates that this commissure does not serve as an alternative route for deviated callosal axons.

Agenesis of Corpus Callosum↗

The overall pattern of ocular dominance bands in cat visual cortex.

This study describes the overall arrangement of geniculocortical input representing the system of cortical ocular dominance bands in layer IV of striate cortex in the adult cat. The pattern of ocular dominance bands was revealed by transneuronal transport of the intraocularly injected tracer wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Our data indicate that this procedure does not damage the retina and that it results in relatively uniform uptake and transport of the tracer. Using previously published techniques (Olavarria and Van Sluyters, 1983, 1985), both cortical hemispheres of each cat were unfolded, flattened and tangentially sectioned. Analysis of the WGA-HRP labeling patterns in these sections revealed a relatively continuous network of irregularly branching bands in layer IV of area 17 in both hemispheres. Because of a systematic difference in the level of interband labeling, ocular dominance bands appear less distinct in the hemisphere contralateral to the injected eye. There is also a tendency for interband labeling to be greater in cortical regions that represent the more peripheral aspects of the binocular portion of the visual field. The width of an individual ocular dominance band in the cat fluctuates, so that it appears to be made up of a series of uniformly sized, roughly circular beads of label. The diameter of these beads averages 667 micron, and preliminary counts indicate that there are 650-675 beads in each striate cortex. Contrary to earlier suggestions, in 4 out of 6 hemispheres analyzed quantitatively there was no tendency for ocular dominance bands to be oriented along a preferred axis in cat striate cortex, including an axis orthogonal to the border between areas 17 and 18. Ocular dominance bands in area 18 appear to be broader than those in area 17, and they seem to have a greater tendency to be oriented orthogonal to the 17/18 border than those in area 17. Compared with the ocular dominance pattern in monkey striate cortex, the ocular dominance pattern in the cat is much less regular. In general, cat ocular dominance bands appear to fluctuate more in width, to change direction more often, and to be less likely to run orthogonal to the 17/18 border. The greater regularity of the primate ocular dominance pattern may be related to differences in the way in which the visual hemifield is mapped onto the striate cortex in these 2 species.

Animals↗

Development of visual callosal connections in neonatally enucleated rats.

The present report extends previous descriptions of the mature distributions of callosal cells and axonal terminations in rats monocularly or binocularly enucleated at birth. It also describes the time course of callosal development in these animals, and establishes the age at which eye removal ceases to alter the normal course of callosal development. Although our results indicate that the callosal pattern is anomalous in adult, neonatally enucleated rats, the major features of the normal callosal pattern are nonetheless clearly recognizable in both monocularly and binocularly enucleated rats. Thus, as in normally reared rats, there are dense accumulations of callosal cells and terminations at the 17/18a border region, at the lateral border of area 18a, and within area 18b in enucleated rats. In addition, several narrow bands of callosal connections bridge the width of area 18a at several rostrocaudal levels, and a ring-like callosal configuration is located anterolateral to area 17. In monocularly enucleated rats, the most prominent anomaly develops in the hemisphere ipsilateral to the remaining eye, where a dense band of callosal connections runs rostrocaudally through the center of area 17. Periodic fluctuations in the density of labeling along the length of this extra band give it a beaded appearance. The callosal pattern in the hemisphere contralateral to the remaining eye in these rats appears normal. Binocular enucleation causes the appearance of discrete regions of reduced labeling within the 17/18a callosal band and several densely labeled tongue-like regions that extend medially from this band well into area 17. The laminar distribution of callosal cells and terminations is not significantly altered by loss of one or both eyes at birth. Our data indicate that enucleation does not affect the time course of callosal development. Thus, in enucleated pups, all features of the mature callosal pattern can be recognized by 6-7 days of age, and by 12 days of age the patterns appear virtually mature. Finally, our data reveal that monocular or binocular enucleations performed at 6 days of age or later allow the callosal pattern to develop normally, whereas enucleations performed between birth and 5 days of age produce anomalies similar to those observed in rats enucleated at birth. Thus, at about 6 days of age--just as the earliest features of the mature callosal pattern become discernible, and long before rats first open their eyes--the developing callosal pathway is no longer susceptible to disruptions of visual input.

Age Factors↗

Organization and postnatal development of callosal connections in the visual cortex of the rat.

The distribution of callosal cells and terminals was studied in the posterior neocortex of pups whose ages ranged from 3 to 16 days and in adult rats 2 months of age or older. Callosal cells and terminations were revealed using retrograde (horseradish peroxidase) and anterograde (horseradish peroxidase; tritiated proline) tracing techniques, respectively, and the distribution of callosal connections was analyzed in tangential or coronal histological sections. In agreement with previous studies, we observed that the pattern of callosal connections in areas 17 and 18 of adult rats contains the following features: (1) a dense band of callosal cells and terminations separating the interiors of areas 17 and 18a, (2) a ringlike configuration anterolateral to area 17, (3) a region of dense labeling lateral to area 18a, (4) several narrow bands of labeling that bridge area 18a at different anteroposterior levels, and (5) one or more labeled regions in area 18b. In all these callosal regions, labeled cells and terminations are densely aggregated in layers II-III, Va, and Vc-VIa, and less densely in layer IV and the remaining portions of layers V and VI. High densities of isotope-labeled fibers are also observed in the lower half of layer I. Throughout the interiors of areas 17 and 18a, a significant number of labeled cells are observed in layers Vc-VIa. In contrast to adult rats, in neonates no distinct tangential pattern of callosal connections is apparent. Instead, labeled cells are densely aggregated in two continuous horizontal bands located in cortical layers Va and Vc-VIa, and callosal axons are largely restricted to white matter. During the first 2 postnatal weeks there is a progressive loss of callosal cells in regions that normally have few callosal cells in the adult (e.g., interiors of areas 17 and 18a) and an increase in the number of cells in layers II-IV in regions that are densely callosal in the adult (e.g., callosal regions at the 17/18a border, lateral border of area 18a, and in area 18b). The decrease in the number of callosal cells in the interiors of areas 17 and 18a is more severe in the upper than in the lower band of the immature labeling pattern, and our data from tangential sections indicate that this loss of callosal neurons occurs synchronously across the interiors of these areas. During this period there is also a localized invasion of labeled callosal axons into those regions of gray matter where they will be found in adult life.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Horizontal optokinetic nystagmus in the cat: recovery from cortical lesions.

We have examined recovery from the acute effects of unilateral and bilateral visual cortex lesions on horizontal optokinetic nystagmus (OKN) in the cat. A single bilateral cortical lesion virtually abolishes monocular OKN in response to temporalward stimulation, and severely reduces OKN in response to nasalward stimulation at higher drum velocities. A unilateral cortical lesion causes deficits in OKN toward the side of the lesion, but these changes are less substantial than those observed after a bilateral lesion. The nature of the acute changes in OKN caused by cortical lesions supports the notion that the visual cortex has two important roles in the OKN system of the cat: first, it mediates OKN in response to temporalward motion of the visual environment during monocular viewing; second, it expands the response range of the OKN system to include higher stimulus velocities. Finally, the results from unilaterally lesioned cats suggest that a single hemisphere can mediate OKN in both directions, with an emphasis on the direction ipsilateral to that hemisphere. The patterns of recovery of OKN in lesioned cats follow two major trends: a small, gradual increase in the overall gain of OKN from its severely depressed level immediately after a large bilateral lesion, and a 'balancing' process that reduces the marked asymmetry between rightward and leftward OKN caused by a unilateral lesion. This balancing of the reflex is accomplished by an improvement in performance in one direction while performance in the opposite direction actually declines. Recovery is faster and more pronounced in lesioned cats with one cortical hemisphere intact, suggesting that the surviving visual cortex compensates for the effects of the lesion by modifying activity in subcortical pathways. These experiments indicate that the visual system of the cat has the capacity to recover at least partially from the deficits in OKN behavior caused by cortical lesions, and that this recovery is the outcome of an interaction between cortical and subcortical pathways mediating this important visuomotor reflex.

Adaptation, Physiological↗

Horizontal optokinetic nystagmus in the cat: effects of long-term monocular deprivation.

The effects of prolonged monocular deprivation (MD) on horizontal optokinetic nystagmus (OKN) have been examined in cats subjected to unilateral or bilateral visual cortex lesions. Presurgically , OKN elicited through the deprived eye was substantially weaker than that through the non-deprived eye. This effect was most prominent for OKN in response to temporalward stimulation, which essentially was abolished in the deprived eye. In addition, OKN elicited by temporalward stimulation of the non-deprived eye tended to be weaker in comparison to nasalward stimulation of that eye. A bilateral cortical lesion severely disrupted OKN behavior through the non-deprived eye but left OKN through the deprived eye relatively unaffected, with the result that the marked interocular differences in OKN that were present presurgically disappeared. During the recovery period following this lesion, there was a small gradual improvement in OKN through both eyes, so that OKN performance through the deprived eye ultimately exceeded that observed presurgically . Unilateral cortical lesions had little effect on OKN through the deprived eye, but they produced substantial changes in OKN through the non-deprived eye. Both the immediate effects of cortical lesions, and the patterns of recovery observed following these lesions, in many ways resemble those observed when normally reared cats are subjected to similar lesions. These behavioral experiments indicate that while subcortical OKN pathways are spared from the effects of long-term monocular deprivation, cortical pathways mediating OKN through the deprived eye are severely disrupted.

Animals↗

Retino-pretectal projections in monocularly deprived cats.

Experiments using double-label anterograde tracers in normally reared and monocularly deprived cats reveal that the overall pattern of retino-pretectal projections appears similar for the deprived and non-deprived eyes of monocularly deprived cats, and no different from that observed in normally reared cats, in terms of both overall extent and amount of binocular overlap. These findings indicate that this pathway is unaffected by prolonged periods of monocular deprivation, suggesting that the presence of binocular overlap per se is not a sufficient condition for binocular competition to occur.

Animals↗

Recovery from effects of brief monocular deprivation in the kitten.

The potential for recovery from the cortical effects of monocular deprivation (MD) was studied in kittens that were briefly deprived and then exposed to various periods of normal binocular vision. In eight kittens, recordings from the hemisphere ipsilateral to the deprived eye revealed that at 4 wk of age, exposure to 12 h of MD (six 2-h sessions spread over 2 days) was sufficient to cause a massive shift in the ocular dominance of striate cortex neurons in favor of the nondeprived eye. Six of these MD kittens were allowed 3 wk of normal binocular vision and then recorded from a second time to assess the extent to which their cortex could recover from the effects of this brief period of deprivation. Data from these animals indicated that now approximately equal numbers of cortical neurons were dominated by each eye and that, while the overall level of binocularity was somewhat lower than that found in normally reared animals, the majority of cells had regained functional binocular connections. The possibility that cortical binocularity could recover even further was explored by allowing four of these six MD kittens to experience an additional 4 wk of binocular vision and then recording from them a third time. These final recordings indicated that following a total of 7 wk of binocular vision, the level of cortical binocularity was no different from that found in normally reared animals. Having demonstrated that normal binocular function can be restored to a cortex in which it had been severely disrupted, we next attempted to characterize the earliest stages of this recovery process by examining the pattern of cortical binocularity in 10 MD kittens that were allowed to experience either 6 or 12 h of binocular vision (given over 1 or 2 days, respectively). Our results indicate that, during the initial day of binocular vision, recovery seems to involve a noncompetitive expansion of functional cortical input from the deprived eye, which joins with input from the nondeprived eye in driving cortical neurons. The level of cortical binocularity continues to increase during the next day of binocular vision, but now there is also a small increase in the proportion of cells driven exclusively by the initially deprived eye--suggesting that there may be an additional competitive component to the early stages of recovery. The results of this study complement our previous report of complete recovery of binocularity following exposure to a brief period of optically induced strabismus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗