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19三体小鼠视觉皮层的产后发育改变。

Altered postnatal development of the visual cortex in trisomy 19 mice.

作者信息

Lorke D E, Albrecht H

机构信息

Abteilung für Neuroanatomie, Universitätskrankenhaus Eppendorf, Hamburg, Germany.

出版信息

Brain Res Bull. 1994;34(6):563-70. doi: 10.1016/0361-9230(94)90141-4.

DOI:10.1016/0361-9230(94)90141-4
PMID:7922599
Abstract

The development of the visual cortex was studied in 30 Trisomy 19 (Ts19) mice aged 1-16 days postpartum and their euploid littermates. Morphogenesis of the Ts19 visual cortex, though delayed in development, followed the regular sequence observed in control littermates. Early morphogenetic events, such as obliteration of the ventricular lumen, disappearance of the ventricular zone, formation of a visible apical dendrite, as well as disappearance of both migrating neurons and the columnar organization of bipolar preneurons were delayed by 1 day; maturation steps occurring later such as appearance and disappearance of perikaryal basophilia were delayed by 2 days. Myelination of the white matter was similarly retarded by 2 days. The fronto-occipital length of the cerebral hemispheres and the thickness of the visual cortex were decreased by about 20%, consistent with a hypoplasia of the Ts19 neocortex. Unlike in the cerebral cortex of human Ts21, morphometric analysis of the visual cortex of Ts19 mice did not give any indication of a selective deficit in a particular neuron population; the increased cell density and the reduced nuclear volume observed during early postnatal development are attributable to a maturational delay. The relevance of these results with respect to the mechanisms underlying neuropathological alterations in human Ts21 is discussed.

摘要

研究了30只出生后1至16天的19三体(Ts19)小鼠及其整倍体同窝小鼠的视觉皮层发育情况。Ts19视觉皮层的形态发生虽然发育延迟,但遵循了在对照同窝小鼠中观察到的正常顺序。早期形态发生事件,如脑室腔闭塞、脑室区消失、可见顶端树突的形成,以及迁移神经元和双极前神经元柱状组织的消失,均延迟1天;后期发生的成熟步骤,如核周嗜碱性的出现和消失,延迟2天。白质的髓鞘形成同样延迟2天。大脑半球的额枕长度和视觉皮层的厚度减少了约20%,这与Ts19新皮层发育不全一致。与人类21三体的大脑皮层不同,对Ts19小鼠视觉皮层的形态计量分析未显示任何特定神经元群体存在选择性缺陷的迹象;出生后早期发育过程中观察到的细胞密度增加和核体积减小归因于成熟延迟。讨论了这些结果与人类21三体神经病理改变潜在机制的相关性。

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