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R D Lund

Publications and source records attributed to R D Lund.

At least 163 records · Page 9Linked to original sources

Normal and abnormal uncrossed retinotectal pathways in rats: an HRP study in adults.

Horseradish peroxidase was injected into the superior colliculus of normal pigmented and albino rats and rats which had been unilaterally enucleated at birth, in order to identify the retinal ganglion cells which contribute normal and abnormal uncrossed retinotectal axons. The results show that while in pigmented rats, the normal uncrossed pathway derives solely from the lower temporal retina and distributes to the anterior and medial parts of the colliculus, occasional cells throughout the retina of albino rats contribute to the uncrossed pathway and the terminal distribution is broader in the tectum. These findings are confirmed with orthograde pathway tracing methods. After neonatal unilateral eye enucleation, many more ganglion cells in the remaining eye of both pigmented and albino rats project ipsilaterally. It is notable from both HRP studies and from further degeneration experiments that cells in part of the lower temporal retina do not restrict their distribution to a mirror togographic position in the ipsilateral tectum but send axons across all but the posterolateral part of the colliculus. No single class of ganglion cell (defined by soma diameter) appears responsible for the expanded ipsilateral projection, although more large cells from the lower temporal retina are involved. These may be the result of enlargement of cells with expanded terminal fields rather than necessarily indicating a preferential contribution from one retinal ganglion cell class.

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Transplantation of embryonic occipital cortex to the brain of newborn rats. An autoradiographic study of transplant histogenesis.

The neurogenesis of immature cerebral cortex transplants was investigated using tritiated thymidine (3HT) autoradiography. Cortical tissue taken from rat fetuses during their last week of gestation (E15-E21) was transplanted to the tectum or cerebral cortex of newborn rat hosts. At different times after transplantation, a single injection of 3HT was given to the host. Most of the experimental animals were killed after the transplants had grown to maturity (5-12 weeks), and some were studied shortly after the tracer had been given. In other experiments, donor tissue was used that was labeled in utero up to 1 day before being transplanted on E16, E17, E18, or E19. It was found that neurons labeled before transplantation survived and differentiated in the graft. Removal of the graft from its natural context did not prevent 3HT incorporation into surviving precursor neurons, indicating continuation of neurogenesis in the cortical transplants. In transplants from E16 donors neurons continued to be generated for 5-6 days after transplantation. Termination of neurogenesis occurred at successively earlier times in transplants taken from correspondingly older embryos. Independent of size and position of the transplant, application of 3HT after "projected" transplant ages of E23 and older labeled only nonneuronal cells. This suggests a time schedule of neuron generation in the cortical transplants similar to that observed during normal development of the cerebral cortex, which is not disturbed by the transplanting procedure.

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Specific projections of retina transplanted to rat brain.

Retinae were taken from fetal rats and transplanted adjacent to the superior colliculus of neonatal rats. After 1 month survival, the transplants were surgically removed from the hosts, locally damaged or injected with horseradish peroxidase (HRP) to determine the distribution of the transplant efferents in the host brains. Histological examination of the transplants revealed cell and plexiform layers characteristic of normal retinae. Since the retinae were undifferentiated at the time of transplantation, this layering developed within the host. The only obvious differences from normal retina were that the layers were organized in rosettes or folded sheets and lacked well developed photoreceptor outer segments. In animals which had lesions or HRP injections confined to the retinal transplant, proper staining of sections of the host brain revealed transplant projections. These projections were confined to the optic tract and nuclei which are normally retinorecipient such as the superior colliculus and dorsal lateral geniculate nucleus. Projections were found along the border of non-retinorecipient nuclei such as the lateral posterior nucleus, but did not appear to enter these nuclei. It was observed that within the superior colliculus the host retinal input had an effect on the distribution of the transplant projection. In one-eyed hosts the transplant projection was distributed throughout the stratum (s.) zonale, s. griseum superficiale, and s. opticum; whereas in the two-eyed hosts, the transplant projection was confined to the s. zonale and the border between x. griseum superficiale and s. opticum. We suggest that a special affinity exists between the axons of the retinal transplants and host visual structures. Furthermore, factors, such as competition and timing may be important in determining the distribution of the transplant axons within the specific target nuclei. Transplantation appears to be a useful technique for further studies on the mechanisms underlying the development of specific neuronal connections.

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Intertectal crossing of optic axons after tectal fusion in neonatal rats.

Surgically-induced fusion of the superior colliculi along the midline was performed in newborn rats to provide a bridge for optic axons from one eye to cross the tectal midline. The results indicate that although tectal fusion is a necessary condition of optic axons to cross from one side of the midbrain to the other, it is not sufficient by itself to induce crossing unless the optic input from the opposite side is also removed. This finding is discussed in relation to tectal lesion studies and is compared with our previous observations of the corticotectal pathway.

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Histogenesis of the superior colliculus of the albino rat: a tritiated thymidine study.

The pattern of generation of neurons in the albino rat superior colliculus has been studied in adult and fetal material. Neurons are generated between embryonic days 12 to 17, with rostrolateral colliculus in advance of caudomedial parts. More of the cells contributing to the deeper layers are generated early, while more of the later generated cells are located superficially. The cells of individual laminae are not formed on specific days as in the cortex, nor are the complicated gradients described previously for the chick optic tectum evident. While the largest cells (found deep in the colliculus) are among the first formed and the small marginal cells among the last, there is in general a broad range of cell size being generated at any one time. The observed patterns are consistent with the concept of simultaneous production of several cell types from the ventricular epithelium on any given day. Studies of material at short times after [3H]thymidine injection allow correlation of the time of arrival of cells in their appropriate layer with time of arrival of afferents. In addition they suggest that factors controlling the final placement of cells in the mature nervous system is a very complex process and may involve some form of intercellular recognition.

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Further studies on the aberrant cross visual corticotectal pathway in rats.

An aberrant crossed corticotectal pathway can be generated by removal of one visual cortex and the contralateral superior colliculus from newborn rats. This aberrant crossed corticotectal projection arises from the pyramidal neurons located in layer V of the visual cortex and terminates in a spatially orderly manner in the appropriate laminae of the cortically deafferented contralateral colliculus. Comparable results cannot be reproduced by unilateral collicular lesions alone. The significance of these findings and the possible mechanisms involved in the formation of the aberrant pathway are discussed and compared with the retinotectal system.

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Development of neurons in the visual cortex (area 17) of the monkey (Macaca nemestrina): a Golgi study from fetal day 127 to postnatal maturity.

The morphological maturation of several varieties of neurons of cortical area 17 have been followed in Golgi Rapid preparations from Macaque monkeys ranging in age from fetal day 127 to maturity. A developmental sequence common to all varieties of neuron is described. Maturation occurs at the same rate at all cortical depths and appears to relate to the size of the neuron rather than to factors such as generation time, arrival at a final laminar position or cell type. The characteristic laminar patterns of cell type distribution and the specific axonal and dendritic arborisations seen in the adult are generated in the earliest stages of growth and do not occur as the result of elimination from a wider, less precise, distribution. During the period from birth to postnatal week 8 a marked increase in the numbers of dendritic spines is seen in all varieties of neuron including those which will be spine-free in the adult. Following this period an equally marked reduction in spine numbers occurs, initially rapid but continuing at a slower rate even nine months postnatally. Possible relationships between these postnatal dendritic spine changes and the extreme sensitivity of the system to visual input during the early postnatal weeks are discussed.

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Development of the geniculocortical pathway in rats.

Most cell of the dorsal laterial geniculate nucleus of rats are generated on fetal days 12 to 14. Their axons invade the telencephalon on fetal day 16 and run in the intermediate zone just below the cortical plate, reaching the visual area of fetal day 18. The axons do not invade the cortical plate significantly until close to birth (day 22 of gestation) and reach their zone of terminal distribution between postnatal days 1 and 4. In subsequent days the projection becomes progressively more heavily distrubuted in layers IV and I, and synapses of thalamic origin can be identified in these layers. While cells destined for layers IV cross the intermediate zone at the time that thalamic axons first arrive, this coincidence of growth does not seem to be a factor which determines the specificity of patterns of thalamocortical connections since the cells reach layer IV several days before the axons. It is unclear why the axons should wait several days in the region immediately below the cortical plate before invading; although there is a parallel in previous studies on the development of the chick retinotectal pathway (Crossland et al., '75).

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Differential central distribution of optic nerve components in the rat.

The distribution of Fink-Heimer positive degeneration and neurofibrillar proliferation has been examined in the dorsal lateral geniculate nucleus (dLGN) and superior colliculus of albino and pigmented rats following enucleation between post-natal days 12 and 30 and as adults. With survival times of 6 h to 5 days following enucleation, the location of maximum degenerative reaction stained by the Fink-Heimer method changes with increasing survival time in both regions. In the dLGN contralateral to the eye removal the earliest degeneration appears in a lamina occupying the medioventral extent of the nucleus and is rapidly removed; later degeneration fills a central lamina of the nucleus with a patch of degeneration extending to the outer surface of the nucleus at the mediodorsal margin. The latest occurring degeneration fills the outermost lamina and is still obvious when degeneration is largely dispersed from the inner and central laminae; this outer lamina shows an early filamentous degenerative reaction in the adult. The uncrossed optic pathway occupies a portion of the central lamina of the nucleus, and in albino animals it shows a rapid degeneration and dispersion similar to the innermost lamina on the crossed side; in the pigmented animals degeneration of the uncrossed projection starts as early as that of the albino but persists as long as the degeneration of the central lamina on the crossed side. The degeneration time of the sprouted, uncrossed pathway resulting from unilateral enucleation at birth is similar in albino and pigmented rats and resembles in timing the normal uncrossed pathway of pigmented rats. These results suggest that there are at least 3 different fiber populations in the rat optic nerve with different distribution in the dLGN. The uncrossed optic pathway of albino and pigmented rats appears to differ in fiber composition; this may relate to aberrations in mapping of uncrossed projections in the albino.

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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.

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Transplanted neural tissue develops connections with host rat brain.

Superior collicular fragments transplanted from fetal to newborn rat brains develop complex internal organization and receive visual afferents from the host providing they lie sufficiently close to the host visual pathways. This system allows investigation in vivo of special affinities between cells of the mammalian central nervous system.

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An aberrant crossed visual corticotectal pathway in albino rats.

This study investigates the dynamic nature of the developing corticotectal pathway arising in the visual cortex. Special attention is given to the interaction occurring between the corticotectal pathways of each side of the brain and between corticotectal and retinotectal terminations. Normally the visual cortex of rats projects only to the ipsilateral superior colliculus. If one visual cortex is removed at birth, the remaining visual cortex subsequently shows a bilateral projection to the superior colliculus. The aberrant corticotectal pathway is heavier if the cortical ablation is accompanied by eye removal at birth but eye enucleation alone is not a sufficient stimulus for production of a crossed corticotectal projection. The aberrant crossed pathway shows a topographic order which appears to correspond to that of the normal ipsilateral corticotectal pathway. The pathway differs from the aberrant projections from the retina in that lesions done as late as 20 days postnatal still result in an aberrant crossed corticotectal pathway. This is similar to the aberrant crossed cortical projections from sensorimotor cortex. The pathway would appear to arise as a result of lack of competition from corticotectal axons normally present contralaterally or from attraction of denervated corticotectal sites. While denervated retinotectal sites stimulate sprouting of the corticotectal axons once in the deafferented colliculus, they do not stimulate crossing of the corticotectal projection.

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