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Objective To analyze the excitotoxicity of monosodium glutamate (MSG) in the offspring cerebral cortex and hippocampal subregions after maternal oral administration of MSG. Methods Kunming mice were given per os MSG ( 4.0 g/kg ) at 17～21 days of pregnancy and their offspring behaviors were studied at 10, 20 , 30 days postnatally. By using immunohistochemical means, the involvement of Bcl-2 and Bax in the glutamate-induced cell death in cortical and hippocampal neurons were examined. Cell damage was assessed by direct cell counting. Results Administration of monosodium glutamate during the fetal period in mice resulted in a moderate increase in the expression of Bax in principal neurons in CA1, CA2, CA3, CA4 and in the cerebral cortex at postpartum 10, 20, 30 days in the offspring mice, whereas Bcl-2 protein expressions were reduced significantly in the same regions as compared with those of controls. Conclusion These findings suggest that glutamate toxicity results in cellular death via an apoptotic mechanism in which the Bcl-2/Bax-alpha molecular complex 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.
Objective To analyze the excitotoxicity of monosodium glutamate (MSG) in the offspring cerebral cortex and hippocampal subregions after maternal oral administration of MSG. Methods Kunming mice were given per os MSG (4.0 g / kg) at 17 ~ 21 days of pregnancy and their offspring behaviors were studied at 10, 20, 30 days postnatally. By usinghistochemical means, the involvement of Bcl-2 and Bax in the glutamate-induced cell death in cortical and hippocampal neurons were examined. Cell damage was assessed by direct cell counting. Results Administration of monosodium glutamate during the fetal period in mice resulted in a moderate increase in the expression of Bax in principal neurons in CA1, CA2, CA3, CA4 and in the cerebral cortex at postpartum 10, 20, 30 days in the offspring mice, Bcl-2 protein expressions were reduced significantly in the same regions as compared with those of controls. Conclusion These findings suggest that glutamate toxicity results in cellular de ath via an apoptotic mechanism in which the Bcl-2 / Bax-alpha molecular complex may be involved. The glutamate-induced apoptosis appears to be related to the modulation of the Bcl-2 family gene products such as Bcl-2 and Bax.