Abnormal Development and Apoptosis Observed in Brains of the Trisomy 16 Mouse
Korean Journal of Pathology
;
: 570-580, 1999.
Artigo
em Coreano
| WPRIM
| ID: wpr-207729
ABSTRACT
We have studied morphologic characteristics and apoptosis on the fetal brain of the trisomy 16 mouse, a model for human trisomy 21 syndrome. This study was based on serial sections of the whole brain from a sample of sixteen trisomy 16 mice and forty-six age-matched control littermates from embryonic day (ED) 12 to ED 18. Trisomy 16 brains showed a reduction of telencephalic size and abnormal cortical development. At ED 13 trisomy 16 and control brains appeared similar. By ED 14 difference in the cortical thickness and telencephalic growth became evident, and by ED 16 a marked size difference had developed between the trisomy 16 and control brains. By ED 18, however, the thickness of the trisomy 16 cortex had increased considerably and was not significantly different with respect to the thickness and cross-sectional areas of the pallium and its constituent cortical layers. The cell density of the trisomy 16 cortex had persistently decreased before ED 17, when the cell density of control and trisomy 16 corteces was similar within each layer. At ED 18 cell density of trisomy 16 cortex in each layer increased. There was inverse relationship between a number of TUNEL positive apoptotic cells and cell density in the trisomy 16 brains. Our results suggest that developmental abnormalities of the trisomy 16 brain indicated developmental delay of the telencephalon growth, which may be caused by apoptosis rather than by a proliferation defect.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Telencéfalo
/
Trissomia
/
Encéfalo
/
Contagem de Células
/
Apoptose
/
Síndrome de Down
/
Marcação In Situ das Extremidades Cortadas
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
/
Humanos
Idioma:
Coreano
Revista:
Korean Journal of Pathology
Ano de publicação:
1999
Tipo de documento:
Artigo
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