Altered postnatal development of the visual cortex in trisomy 19 mice.
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.
Lorke
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Abteilung für Neuroanatomie, Universitätskrankenhaus Eppendorf, Hamburg, Germany.
Albrecht
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H
D000818:Animals; D004314:Down Syndrome / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008815:Mice, Inbred Strains; D009024:Morphogenesis; D014314:Trisomy / Q000503:physiopathology*; D014793:Visual Cortex / Q000254:growth & development* / Q000473:pathology