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Biomedical subjects

B L Finlay

Publications and source records attributed to B L Finlay.

At least 37 records · Page 2Linked to original sources
PubMed1989

Differential elasticity of the immature retina: a contribution to the development of the area centralis?

Differential stretch of a retinal surface with an initially uniform cell density has been repeatedly implicated as one of the developmental mechanisms that produces the topographic organization of cell density in the adult retina, notably the area centralis or visual streak versus peripheral regions. It is known that intraocular pressure is required to produce the normal conformation and thinning of the retina during development. We tested the possibility that the retina has elastic properties that might permit differential stretch in conjunction with intraocular pressure. The relative deformation of the retina containing the presumptive area centralis was compared to the deformation of peripheral retina at equivalent applied fluid displacements in 7-12-day-old cats. The peripheral retina deformed significantly more, consistent with the hypothesis that differences in the local elasticities of the developing neural retina contribute to its characteristic topographic changes. Thus, a biomechanical property of the growing eye may contribute to the mechanism by which the pattern of the visual array is sampled.

Animals↗
PubMed1989

Conservation of receptive-field properties of superior colliculus cells after developmental rearrangements of retinal input.

The formation of topographic maps requires not only that afferents synapse with the appropriate targets, but that the spatial relationships between the afferents be maintained. During development, in addition to the formation of the topographic map, the connectivity patterns responsible for the receptive-field properties of the target cells are being formed. The extent of interaction between these two processes is unknown. The present study addresses this question by manipulating afferent/target ratios during development, thus altering the topography of the map, and studying the effects of this alteration on the receptive-field properties of single target cells in the adult. Partial unilateral lesions of the superior colliculus (SC) were made in neonatal hamsters. These lesions result in a compression of the retinotopic map onto the remaining collicular fragment. Single cells were recorded from the superficial gray layer of the SC in the adult in response to visual stimuli. Receptive-field properties observed in lesioned animals were compared to those in normal animals and in sham operates. Receptive-field properties were largely unaffected by the change in the topographic map. There was no difference in the receptive-field size of single tectal cells of lesioned and unlesioned animals. Stimulus velocity and stimulus size tuning functions remained the same. This raises the possibility that, rather than the expected increase in convergence of retinal ganglion cells (RGC) onto single collicular cells, single SC cells receive input from ganglion cells representing the same amount of retinal area as in unlesioned animals. The excess ganglion cells created by the partial target removal would then project elsewhere and/or reduce their arbor within the SC. Regardless of the mechanism, it is clear from our results that circuitry in the retinotectal system of the hamster can compensate for conditions of increased afferent availability and thus maintain receptive-field properties.

Animals↗
PubMed1988

Control of cell number in the developing neocortex. I. Effects of early tectal ablation.

Target availability is an important factor in the early control of neuron number in many structures in the developing vertebrate nervous system. In early neocortical development, the role of target availability in the survival of subcortically projecting neurons is not yet understood, particularly because these cells' axons are widely distributed and highly branched. In this study, we have looked for alterations in the pattern of early cell death, adult cell density and adult morphology of pyramidal cells in layer V of visual cortex consequent to removal of one of their principal targets, the ipsilateral superior colliculus. After neonatal tectal ablation, there was no difference in the incidence of pyknotic cells in the cortex overall, or in layer V during the period of normal cell death in the cortex. Neither in adulthood, nor at any point in development did the density of layer V cells or cortical cell density overall differ from normal in Nissl material. Soma size of cells in layer V overall did not differ from normal in Nissl material. In addition, the soma size of the subpopulation of cells labelled with horseradish peroxidase (HRP) from midbrain injections was unaltered. In summary, this cell population appears unresponsive in both number and morphology to deletions of a major component of its target pool. This observation has some interesting implications for reasons of constancy of cell number in layer V across cytoarchitectonic areas.

Aging↗
PubMed1988

Control of cell number in the developing neocortex. II. Effects of corpus callosum section.

To determine if cell death participates in the regulation of cell number between interconnecting populations of the neocortex, we sectioned the corpus callosum of neonatal hamsters, thus depriving callosally projecting cells of their normal targets and callosally-recipient cells of their normal afference. The numbers of neurons per unit column in two areas of the cortex which have heavy callosal projections (the 17-18a border and area 6) and one area that is relatively acallosal (area 3) were compared in animals with early corpus callosum sections and controls. No differences were found, either for a 'unit cortical column,' or for the callosally-projecting layers (II-III and V). Mean soma sizes in layers II-III and V of all three areas were likewise unchanged. In area 6 and part of area 3, however, the distribution of soma sizes in callosally projecting and recipient laminae was significantly altered. The change in size distribution without change in mean soma area suggests that the cortex responds to the elimination of the callosal pathway in more than one way. Since no role for cell death in removal of diffuse connectivity or in target regulation of neuron number has yet been found, a new hypothesis for the function of cell death in local cytoarchitectural differentiation of the cortex is proposed.

Aging↗
PubMed1988

Development of ganglion cell topography in ferret retina.

The adult ferret has approximately 90,000 retinal ganglion cells, arranged in a prominent area centralis and visual streak. The role of differential cell generation, cell death, and retinal growth in the control of adult retinal ganglion cell number and distribution was evaluated by examining basic aspects of retinogenesis, including growth in retinal area, developmental changes in the number, size, and distribution of retinal ganglion cells (identification aided by retrograde transport of HRP), and the incidence of degenerating cells in the ganglion cell layer. Retinal development in the ferret was also compared to retinal development in the cat (which has an even more differentiated area centralis) to determine what alterations of developmental parameters are most closely associated with this species difference in adult morphology. The area of the retina increases linearly from birth (12 mm2) to postnatal day 24 (54 mm2), reaching an eventual adult value of 64 mm2. Ganglion cell numbers peak at 155,000 (approximately twice the adult number) on postnatal day 3, and fall to adult numbers by postnatal day 6. The remaining cells of the ganglion cell layer, principally displaced amacrine cells, reach their peak number on postnatal day 10 (approximately 280,000), falling to 200,000 by adulthood. Degenerating cells are abundant in the ganglion cell layer in the immediate postnatal period. A difference in the incidence of degenerating cells in the presumptive area centralis versus that in the retinal periphery was not observed postnatally, though there were other striking spatial nonuniformities, suggesting that differential cell loss might contribute to other features of retinal topographic organization. Ganglion cell density is virtually uniform across the retina at birth. Cell density is first reduced in the dorsal retina, resulting in a dorsal-to-ventral gradient in cell density that persists until day 10, when ganglion cell number has stabilized. By postnatal day 24, an area centralis and visual streak has emerged, but not of adult magnitude. Because ganglion cell number has stabilized long before the area centralis and visual streak emerge, we conclude that differential retinal growth is the principal mechanism producing this feature of retinal topography. Comparison with the cat suggests that the proportionately greater nonuniform growth of the cat's eye accounts for the greater differentiation of its area centralis.

Algorithms↗
PubMed1987

Regressive events in brain development and scenarios for vertebrate brain evolution.

The problems of the evolution of varying brain size, the specialization of particular functional systems and overall differences in the relative complexity of brain organization are discussed in terms of alterations of regressive events in neurogenesis (cell death and axon retraction). Three scenarios for evolution, cascade reorganization, parcellation and heterochrony, are considered in light of regressive mechanisms during development.

Animals↗
PubMed1986

Cell generation, death, and retinal growth in the development of the hamster retinal ganglion cell layer.

During the early postnatal period in the hamster, the retinal ganglion cell layer grows, establishes its central connections, and undergoes substantial cell loss. In this study, we describe the development of the retinal ganglion cell layer with particular attention to the creation of local specializations in cell density. Changes in the number and spatial distribution of cells identified by a single 3H thymidine injection were examined through the period of maximal cell loss (postnatal days 4-10) and at adulthood. The cells of the retinal ganglion cell layer are generated from embryonic day 10 to postnatal day 3. Overall, cell number in the ganglion cell layer increases by approximately 108,000 cells (223%) from postnatal day 1 to 5, because of continued migration of cells generated prenatally. Cell number decreases from postnatal day 5 to 10 (25%), coincident with the presence of degenerating cells. Cell type is correlated with day of generation: the largest cells, all having retinal ganglion cell morphology, are generated on embryonic days 10 and 11; intermediate-sized cells predominantly of ganglion cell morphology on embryonic day 12; and smaller cells of displaced amacrine or glial cell morphology thereafter. At adulthood, the hamster retina shows a streaklike elevation of cell density through central retina. However, at the time of maximal cell number (postnatal day 5), cell density is uniform across the retina. During the period of cell degeneration, cells are lost in greater relative numbers from the retinal periphery. This cell loss occurs principally from the first-generated cells (embryonic days 10 and 11), as shown by both changes in the distribution of labeled cells and by the spatial pattern of labeled degenerating cells. From postnatal day 10 to adulthood, relative cell density continues to decline in the periphery of the retina, thus suggesting that differential growth completes the production of the adult cell density distribution.

Animals↗
PubMed1986

Control of cell number in the developing visual system. I. Effects of monocular enucleation.

Monocular enucleation of hamsters on the day of birth caused an increase in cellular degeneration and a corresponding loss of cells in the dorsal lateral geniculate nucleus contralateral to the enucleation over the first 12 postnatal days. The superficial layers of the contralateral superior colliculus showed a similar increase in cell degeneration, except rostrally where the remaining ipsilateral projection is found. No changes in degeneration were found in either the ipsi- or contralateral ventral lateral geniculate nuclei, the intermediate and deep layers of the superior colliculus, or in the dorsal lateral geniculate and superficial superior colliculus ipsilateral to the enucleation, even though all were denervated to some degree. The disparities in the incidence of degenerating cells normally seen in the central and peripheral regions of the superior colliculus and dorsal lateral geniculate were preserved following the monocular enucleation. The incidence of degenerating cells in early development correlates well with known alterations in adult cell number. Only major denervations of retinal targets appear to be adequate to produce measurable changes in early cellular degeneration.

Animals↗
PubMed1986

Control of cell number in the developing visual system. II. Effects of partial tectal ablation.

The effects of potential excess innervation on cell survival in the superior colliculus and related structures during the period of normally occurring cell death was examined. A unilateral, partial lesion of the superficial layers of the superior colliculus on the day of birth, which results in a compression of the retinotectal map into the remaining area, was the manipulation used to produce the potential excess innervation. Cell density was reduced in the tectal fragment early in development, consistent with hyperinnervation, but had returned to normal by the end of the period of normally occurring cell death. The overall incidence of cell degeneration in the remaining partial colliculus was not different from the undamaged contralateral colliculus or from normal, though there was evidence of a transitory depression and later elevation of cell loss. Cell loss in the retina contralateral to the lesion was increased in the late part of the period of normal cell loss and there were fewer cells in the retinal ganglion cell layer at maturity. The amount of the cell loss in the retina was small compared to the amount of target removal. These results suggest that the survival of neurons with branching axons does not sensitively reflect target availability.

Animals↗
PubMed1986

Control of cell number in the developing visual system. III. Effects of visual cortex ablation.

The effect of unilateral deletion of the visual cortex on early cell death and eventual cell number in various structures of the visual system was examined. At minimum, this manipulation potentially provides excess retinal afference to the superior colliculi, partially denervates the superior colliculi, reduces normal retinal terminal area and opens up potential target space for the retina and superior colliculus in those areas where they share terminal space with the visual cortex. All layers of the superior colliculus, bilaterally, showed an initial decrease in the rate of cell death relative to normal followed by an increase in cell death rates. No change in the number or distribution of cells in the retinal ganglion cell layer resulted despite a substantial loss of retinal terminal area, and a substantial alteration of the pattern of retinal central termination. These results are interpreted as evidence for two stages in normally occurring cell death, a first in which axons compete to colonize any available terminal space, and a second in which axon-to-target specificity must be matched. These results also provide evidence that the amount of target required for neuron survival is clearly variable.

Animals↗
PubMed1985

Regional differences in normally occurring cell death in the developing hamster lateral geniculate nuclei.

Normal cellular degeneration occurs in the lateral geniculate nuclei (LGN) of the hamster thalamus early in postnatal development. Degenerative debris can be observed in the ventral and dorsal nuclei at postnatal days 2-10 and is present in greater and more variable amounts in the ventral nucleus. Cell degeneration in the dorsal LGN is maximal at postnatal day 5, identical to the degeneration pattern of the hamster retina and superior colliculus, but shows a second peak at postnatal day 8 which may relate to the establishment of cortical connectivity. The incidence of degenerative debris is significantly higher in the peripheral margins of the dorsal nucleus, a pattern also seen in the retina and the superior colliculus, suggesting that a differential cell death may be involved in the formation of regional specializations in the visual system.

Animals↗
PubMed1985

Temporal retina is preferentially represented in the early retinotectal projection in the hamster.

Retrograde transport of horseradish peroxidase (HRP) after complete transection of the brachium of the superior colliculus on the day of birth in hamsters revealed preferential labelling of the temporal retina. Cytochrome oxidase staining of the retina showed similar preferential temporal labelling. A discrete lack of label of the extreme temporal periphery of the retina contralateral to the HRP placement and a complementary label of ipsilateral temporal periphery were also observed.

Animals↗
PubMed1983

Increased cell number in the adult hamster retinal ganglion cell layer after early removal of one eye.

In hamster, following removal of one eye on the day of birth the amount of normally occurring degeneration in the retinal ganglion cell layer of the remaining eye is reduced, particularly in the temporal retina. To examine the changes in the number and distribution of cells indicated by the alterations in early cell degeneration, adult retinas from hamsters who had one eye removed at birth were compared to those of normal adults. Normal adult retinal ganglion cell layers were found to contain an average of 157,223 cells (a population which includes retinal ganglion cells, "displaced" amacrine cells, and glia). At adulthood, the remaining retinas of early enucleates had an average of 169,863 cells in the ganglion cell layer, an increase of 8%. If only cells having Nissl substance and a soma diameter in excess of 10 micron (a group likely to consist entirely of retinal ganglion cells) are considered, the increase observed was 19%. Cells having Nissl substance and soma diameters between 5 and 10 micron, a group which includes both retinal ganglion cells and displaced amacrines, show a 13% change. Cells less than 10 micron with no Nissl substance visible, which include displaced amacrines and glial cells showed no net change (75,883 versus 75,409). The increase in cell number was found across the entire retina, but was largest in the temporal retina. These results show that alteration in early neuronal survival is a component of early plastic changes in the central nervous system, and that early cell degeneration rates are good predictors of later cell number and distribution.

Animals↗
PubMed1983

Cell degeneration in early development of the forebrain and cerebellum.

The hippocampus, dentate gyrus, cerebellum, amygdala and caudate were examined for degenerating cells in normal neonatal hamsters. Each structure was studied from postnatal day 5 (P5) to P 10. The cerebellum was also studied on P 12. This time span was chosen to coincide with cessation of migration and establishment of connectivity in these structures. Substantial numbers of pycnotic cells were found in all structures except the dentate gyrus. The timing and amount of cell death varied between structures. Both the caudate nucleus and the amygdala showed greater cell losses in their peripheral margins than in their centers. The deep half of the internal granule cell layer of the cerebellum showed greater cell loss than the superficial half on all postnatal days studied.

Amygdala↗
PubMed1982

Cell death in the mammalian visual system during normal development : I. Retinal ganglion cells.

Degenerating cells may be observed with light microscopy in the hamster retinal ganglion cell layer during early postnatal development. On the first postnatal day, degenerating cell profiles were found at a rate of 2.7 per 1,000 live cells. This rate increased to a peak of 14.7 degenerating cells per 1,000 live on postnatal day 5 and then slowed to 4.2 per 1,000 live by postnatal day 10. These rates of cell death correspond to a 49% reduction in cell number in the ganglion cell layer. Examination of the spatial pattern of cell death revealed that although on visual inspection degenerating cells appear to occur in clumps, statistical analysis demonstrated a random distribution within renal areas. Across the retina, cell death rates were higher in peripheral retina than in central retina. The timing and pattern observed correspond well with that of cell degeneration observed in the superficial layers of the superior colliculus, the major target of the retinal projection.

Age Factors↗
PubMed1982

Cell death in the mammalian visual system during normal development: II. Superior colliculus.

Degenerating cells may be observed with light microscopy in the hamster superior colliculus during early postnatal development. In the superficial gray layer and stratum opticum, 1.8 degenerating cells for each 1,000 live cells could be seen on the first postnatal day. This rate increased to 5.6 degenerating cells per 1,000 live cells by postnatal day 8. The rate of cell degeneration was consistently elevated at the medial, lateral, and caudal margins of the superficial gray layer relative to the center. In the intermediate and deep gray layers, the rate of cell death was consistently higher, starting at three degenerating cells per 1,000 on postnatal day 5, and declining to 4.7 per 1,000 by postnatal day 8. In contrast to the superficial gray layer, the number of degenerating cells in the central versus peripheral segments of the intermediate and deep gray layers was quite similar. Although the rate of observable degeneration is low, the likely rapid clearance of degenerating cell debris indicates a substantial loss of cells from the midbrain tectum in early development. The time course of observable degeneration, the amount, and the distribution of degenerating cells are quite similar in the tectum, and its major innervating structure, the retina.

Age Factors↗