Bax-induced apoptosis not demonstrated in the congenital toxoplasmosis in mice.

A prominent neuropathological change observed in a murine model of congenital toxoplasmosis is cerebral cortical hypoplasia. In the early embryonic life of toxoplasmosis mice, the number of apoptotic cell observed in cerebral cortex is increased, indicating that increased number of apoptotic cells might relate to the pathogenetic mechanism of the cortical hypoplasia. Immunohistochemical expression of apoptosis-related factors, Bcl-2 and Bax has been studied in fetal murine brains infected with toxoplasma and in controls. Paraffin sections of the fetal brains on embryonic day (ED) 10, 12, 14, 16 and 18 were applied for the immunostains of Bcl-2 and Bax. Totally, 47 experimental animals (ED10: n=8, ED12: n=6, ED14: n=12, ED16: n=6, ED18: n=15) and 48 control animals (ED10: n=6, ED12: n=8, ED14: n=9, ED16: n=9, ED18: n=16) were examined. Bcl-2 positive cells were detected on ED10, whereas Bax positive cells appeared on ED14. No difference of Bcl-2 and Bax expression between toxoplasmosis and control groups was detected, suggesting that there is no clear relation between Bax-induced apoptosis and cortical dysplasia in congenital toxoplasmosis.