EXPRESSION OF BAX AND BCL-2 IN MOUSE OFFSPRING BRAIN AFTER MATERNAL ORAL ADMINISTRATION OF MONOSODIUM GLUTAMATE

Ｇｌｕｔａｍａｔｅｅｘｃｉｔｏｔｏｘｉｃｉｔｙｐｌａｙｓａｋｅｙｒｏｌｅｉｎｔｈｅｉｎｄｕｃｔｉｏｎｏｆｎｅｕｒｏｎａｌｃｅｌｌｄｅａｔｈｏｃｃｕｒｒｉｎｇｉｎｍａｎｙｎｅｕｒｏｐａｔｈｉｅｓ.Ｂａｘ ,ａｐｒｏ ａｐｏｐｔｏｔｉｃｇｅｎｅｏｆｔｈｅＢｃｌ 2ｆａｍｉｌｙ ,ｈａｓｂｅｅｎｓｈｏｗｎｔｏｂｅｉｎｖｏｌｖｅｄｉｎｄｅｖｅｌｏｐｍｅｎｔａｌｎｅｕｒｏｎａｌｄｅａｔｈ .Ｎｅｕｒｏｎａｌｄｅａｔｈｆｏｌｌｏｗｉｎｇｅｘｃｉｔｏｔｏｘｉｃｄａｍａｇｅｈａｓｂｅｅｎｔｈｏｕｇｈｔｔｏｒｅｆｌｅｃｔｎ…

EXPRESSION OF BAX AND BCL-2 IN MOUSE OFFSPRING BRAIN AFTER MATERNAL ORAL ADMINIS TRATION OF MONOSODIUM GLUTAMATE

Objective To analyze the excitotoxicity of monoso dium glutamate (MSG) in the offspring cerebral cortex and hippocampal subregions after maternal oral administration of MSG. Methods Kunming mi ce were given per os MSG ( 4.0 g/kg ) at 17～21 days of pregnancy and their offs pring behaviors were studied at 10, 20 , 30 days postnatally. By using immunohis tochemical means, the involvement of Bcl-2 and Bax in the glutamate-induced c ell death in cortical and hippocampal neur ons were examined. Cell damage was assessed by direct cell counting. Res ults Administration of monosodium glutamate during the fetal period in mice resulted in a moderate increase in the expression of Bax in principal neuro ns in CA1, CA2, CA3, CA4 and in the cerebral cortex at postpartum 10, 20, 30 day s in the offspring mice, whereas Bcl-2 protein expressions were reduced signif icantly in the same regions as compared with those of controls. Conclusi on These findings suggest that glutamate toxicity results in cellular d eath via an apoptotic mechanism in which the Bcl-2/Bax-alpha molecular comple x may be involved. The glutamate-induced apoptosis appears to be related to the modulation of Bcl-2 family gene products such as Bcl-2 and Bax.