Biomedical subjects

B L Finlay

Publications and source records attributed to B L Finlay.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Thalamic ablations and neocortical development: alterations in thalamic and callosal connectivity.

Corticofugal pathways (callosal, intracortical, and subcortical) have initial axon outgrowth to many areas where no adult connections will persist. Corticofugal projections also demonstrate considerable reorganization after early damage. At the level of gross projections from specific thalamic nuclei to cortical cytoarchitectonic areas, early thalamocortical projections appear to show greater specificity for their targets than do corticofugal projections, and their potential for reorganization after early damage is not known. In this article, we explore the nature of the reorganization shown by the thalamocortical system after early thalamic lesions, and contrast it with reorganization of the origin of contralateral visual callosal projections in the same animals. Hamster pups were given electrolytic lesions in the posterior thalamus on the day of birth, damaging principally either the ventrobasal (somatosensory) or the dorsal lateral geniculate (visual) nucleus. After 30 d of age, HRP was implanted in either the somatosensory or the visual cortex, matching the area of implant with the intended thalamic lesion. The thalamus was reconstructed to determine the remaining nuclei, and the distribution of retrogradely labeled cells was plotted. For animals with HRP implants in visual cortex, the location of callosally projecting cells from the contralateral cortex was charted. These animals were compared to a group of normal adult animals with HRP implants approximately matched for size and location. In seven of eight adult animals with neonatal thalamic lesions, the remaining thalamus did not reorganize to innervate the thalamically denervated cortex. In contrast, the callosal projections from the contralateral visual cortex showed a wider tangential origin in the experimental animals compared to the controls. This expanded callosal projection included cells from temporal cortex, a projection not seen in normal animals. Thus, thalamocortical and callosal projection systems differ in both the magnitude and the nature of their reorganization after early damage.

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PubMedDate not supplied

Dual fate of subplate neurons in a rodent.

While subplate neurons are lost in the development of the cerebral cortex of other mammalian species that have so far been investigated, in rodents the subplate (alternately termed layer VIb or VII) persists to adulthood, at least in part. We traced the developmental course of the subplate in the golden hamster, using two methods. We first used tritiated thymidine labeling to trace relative changes in the numbers of identified cohorts of cells in the subplate, layer VI, and the LGN. We also estimated the total number of cells in the subplate versus layer VI of the cortex from early in development to adulthood. These methods showed a high rate of cell loss in the subplate, between 50% and 80%, but with the clear retention of a substantial fraction of this early-generated population as a recognizable layer in adulthood. Species variations in the timing of cortical neurogenesis and the relative amount of cell loss in the subplate can be used to better describe the developmental function of this region.

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PubMedDate not supplied

Cortical target depletion and the developing lateral geniculate nucleus: implications for trophic dependence.

The dependence of the developing dorsal lateral geniculate nucleus (LGd) on visual cortex for survival has been well documented. Complete removal of visual cortex during early postnatal development results in degeneration of the LGd. To further explore the nature of this trophic relationship, we depleted variable proportions of the principal targets of geniculocortical axons, layer IV neurons, and also variable proportions of the supragranular neurons by intraperitoneal injections of different dosages of a mitotic inhibitor MAM (methylazoxymethanol acetate) into pregnant hamsters at the time when these neurons were being generated in the ventricular zone. We demonstrate that after more than 75% loss of layer IV there is no reduction in cell number in the LGd. HRP (horseradish peroxidase) injections into the LGd in adult animals reveal an essentially normal pattern of termination without evidence of rerouting of geniculocortical axons to other cortical areas, nor compensatory increase in arborization in layer VI and VIb (subplate). Geniculocortical axons terminate principally in the middle stratum of the depleted cortex above layer V, with obvious reduction in both the extent and density of arborization. After higher dosages of MAM treatment resulting in more severe cell loss in layers II-IV with the apparent loss of layer IV, the extent and density of geniculocortical arborization are further reduced. Reduction in size as well as total number of geniculate neurons become detectable. Above depletions of 75% of layer IV neurons, the number of surviving LGd neurons is linearly related to the total number of remaining layer II-IV neurons in the cortex. These findings are discussed in light of the possible trophic mechanisms that match cell populations in number during development.

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PubMedDate not supplied

Cortical target depletion and ingrowth of geniculocortical axons: implications for cortical specification.

During the early development of the neocortex, thalamocortical axons arrive potentially in time to instruct migrating cortical neurons in several aspects of local differentiation, such as number of layer IV neurons and efferent connectivity. Migration of layer IV neurons into the cortical plate just precedes thalamocortical invasion, suggesting that these neurons could cue or tropically direct thalamic ingrowth. To explore the interactions of layer IV neurons and their thalamocortical input, we administered a mitotic inhibitor methylazoxymethanol acetate (MAM) intraperitoneally to time d pregnant hamsters on E14 when layer IV neurons are normally being generated in striate cortex. Reduced numbers of cortical neurons overall, the absence of small diameter granule neurons, and the absence of the zone of reduced density of callosally projecting neurons suggest that neither the depletion of layer IV cells in the ventricular zone nor thalamic afferents in the subplate or cortical plate respecify the later generated cohort of neurons (presumptive layer II/III neurons) to acquire morphological and connectional properties of layer IV. Dil injections into the dorsal lateral geniculate nucleus (LGd) of animals from embryonic (E15) and postnatal (P7) ages show that the final position of thalamic axons with respect to layer V is not affected by the absence of E14 neurons. In the normal visual cortex, geniculocortical axons have begun their arborization in their presumptive target layer in the upper cortex immediately below the undifferentiated cortical plate on P4, while in MAM animals, this process occurs 1 d later. The extent and density of arborization is much reduced in the thinner cortex of the MAM animals. We thus find no evidence for instruction of migrating neurons by thalamocortical axons to assume the layer IV phenotype; if instruction does occur, it must take place in a very restricted time window. Thalamic axons can also find their laminar position in the absence of cells of this phenotype.

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