A chronologic study of apoptotic cells in the cerebral hypoplasia induced by intra-uterine infection

弓形虫感染的胎儿大脑中的一种发育障碍是皮质发育不全，细胞凋亡可能在其过程中起作用。在妊娠第5天（E5），将弓形虫（ME 49株）腹腔注射给妊娠小鼠（C57 BL/6CrSlc），诱导小鼠先天性弓形虫病。在E10、E12、E14、E16和E18，用原位末端标记（TUNEL）方法在感染组和对照组的脑层中显示凋亡细胞。感染小鼠的大脑皮层比对照组薄，并显示出不成熟的层状结构。凋亡细胞主要分布于室管膜下层，中间带偶见。额叶凋亡细胞计数。对照组细胞计数为1.67 ± 0.01。E10为1.00（n=9），E10为1.88（]SY. E12为0.99（n=8），E12为1.83（n = 8）。E14为1.17（n=6），E14为1.44（n = 6）。E16为1.75（n=16），SY为1.56（n = 16）。E18时为1.32（n=16），感染组为3.63（n = 16）。[）3.70（n=8），3.50（]SY. ±. [] 1.76（n=6），3.08（]SY. ±. [] 2.11（n=12），2.18（]SY. ±. [] 2.40（n=11）和1.00（]SY. ±. [] 1.71（n=16）。除E12外，两组小鼠个体间差异显著，统计学显著性较低（p<0.05）。总之，在感染的brians中凋亡细胞的数量增加可以先于对照组。这一证据表明，细胞损伤可能是由于直接原虫感染胎儿脑或受感染母亲胎盘炎的缺血性影响，因此，皮质发育不全将被诱导。

One of the developing disorders in the fetal brain with toxoplasma infection is cortical hypoplasia to which apoptosis may contribute in its process. Congenital toxoplasmosis was induced by intra-peritoneal injection of Toxoplasma gondii (ME49 strain) to the pregnant mice (C57BL/6CrSlc) on gestational day 5 (E5). On E10, E12, E14, E16 and E18 apoptotic cells were demonstrated in the cerebral layrs in both infected and control groups using an in situ end-labeling (TUNEL) method. The cerebral cortex in the infected mice was thinner than in the controls and disclosed an immature laminar architecture. Apoptotic cells distributed mainly in the subependymal layr and occasionally in the intermediate zone. Numbers of the apoptotic cell were counted in the frontal lobes. The cell counts in the control group were 1.67(]SY.+-。[)1.00 (n=9) on E10,1.88(]SY.+-。[)0.99 (n=8) on E12,1.83(]SY.+-。[)1.17(n=6) on E14,1.44(]SY.+-。[)1.75(n=16) on E 16 and 1.56(]SY.+-。[)1.32(n=16) on E18, and in the infected group 3.63(]SY.+-。[)3.70(n=8), 3.50(]SY.+-。[)1.76 (n=6), 3.08(]SY.+-。[)2.11(n=12), 2.18(]SY.+-。[)2.40(n=11) and 1.00(]SY.+-。[)1.71(n=16), respectively. There were considerable differences among individual mice in both groups and statistically a low significance except on E12 (p<0.05). In conclusion an increased number of apoptotic cells in the infected brians could be preceded to that in the controls. This evedence suggests that cell damage might be resulted by a direct protozoal affection to in the fetal brain or by an ischemic influence from placentitis of the infected mother and, therefore, cortical hypoplasia would be induced.