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Cerebellar malformation obtained in rats by early postnatal treatment with 6-aminonicotinamide. Role of neuron-glia interactions in cerebellar development

Identifieur interne : 000586 ( France/Analysis ); précédent : 000585; suivant : 000587

Cerebellar malformation obtained in rats by early postnatal treatment with 6-aminonicotinamide. Role of neuron-glia interactions in cerebellar development

Auteurs : C. Sotelo [France] ; J. P. Rio [France]

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Mots-clés :

Abstract

To analyze the role of neuron-glia interactions during the organogenesis of the rat cerebellar cortex, the glial cells were damaged by the gliotoxic agent 6-aminonicotinamide. A single intraperitoneal injection in newborn rats produced a specific necrobiotic lesion of astrocytes and oligodendrocytes, but spared glial precursors. To allow the development of the cerebellar cortex in a situation in which most of the glial cells were damaged, 6-aminonicotinamide was injected several times during the first two postnatal weeks. Rats were killed at ages ranging between 6 and 26 days. In the youngest animals the lesion was very selective: Bergmann fibers, astrocytes and oligodendrocytes were necrotic or in an advanced stage of hydropic degeneration. Under these circumstances, granule cells were able to migrate. This migration occurred along the surface of severely altered Bergmann fibers. In rats aged 12–14 days the lesion was less selective; in addition to the glial damage, numerous pyknotic cells were observed among immature neurons of the external granular layer. Spared granule cells were still able to migrate, moving along necrotic Bergmann fibers. However, the migration was uneven; in a few folia, independent of the severity of the glial lesion, granule cells were stopped in their migration at the level of the Purkinje cell layer. This incomplete migration resulted in an inversion of the layering, Purkinje cells being adjacent to the white matter. In the oldest rats studied, a remnant of the external germinal layer was still present and the white matter was almost completely devoid of myelinated fibers. In most of the folia the layering was normal, although numerous ectopic granule cells were dispersed throughout the molecular layer. In a few folia, the inversion of the layering remained. At their level Purkinje cells have grown in an abnormal cellular environment. These cells exhibited altered patterns of dendritic arrangements, as well as disturbances in their synaptic investment (mossy fibers directly synapsed on Purkinje spines).These results demonstrate that, in spite of severe Bergmann fiber degeneration, granule cells are able to migrate. In addition, the analysis of Purkinje cells which have grown in an abnormal cellular milieu supports the view that local interactions are necessary to achieve the normal branching of their dendritic tree, and their synaptic investment.


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DOI: 10.1016/0306-4522(80)90092-5


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