Background It is a common phenomenon that children experience multiple general anesthesias in clinical practice, which raises the question whether repeated exposure to general anesthetics would interfere with the deve...Background It is a common phenomenon that children experience multiple general anesthesias in clinical practice, which raises the question whether repeated exposure to general anesthetics would interfere with the development of the central nervous system of children. The present study was designed to evaluate the effects of repeated treatment with ketamine or midazolam on postnatal dendrite development by examining the morphology of the dendritic spines of the pyramidal neurons in the hippocampal CA1 region in mice. Methods The transgenic green fluorescent protein-M line （GFP-M） mice were used in this study. Ketamine （100 mg/kg） midazolam （50 mg/kg） or saline （10 ml/kg） was administered intraperitoneally once a day on consecutive days from postnatal day 8 （P8） to postnatal day 12 （P12）. At postnatal day 13 （P13） and postnatal day 30 （P30）, the density and length of the apical dendritic spines of the pyramidal neurons in the hippocampal CA1 region were examined under a confocal microscope. Results At P13, for both the ketamine group and the midazolam group, the dendritic spines were found with a comparatively lower density and longer average length than in the control group. At P30, no significant difference in the density or average length of dendritic spines was found between the anesthetic group and control group. Conclusions This study indicated that repeated exposure to ketamine or midazolam in neonatal mice impaired dendritic spine maturation immediately afterwards, but this influence seemed to disappear during further postnatal development.展开更多
Polybrominated diphenyl ether (PBDE) is a persistently environmental pollutant ubiquitously found in wildlife and humans. Although concern on PBDE’s toxic effects is steadily increasing, its action on the central ner...Polybrominated diphenyl ether (PBDE) is a persistently environmental pollutant ubiquitously found in wildlife and humans. Although concern on PBDE’s toxic effects is steadily increasing, its action on the central nervous system (CNS) remains largely unknown. To address this issue, the present study ex- amined the development inhibition of PBDE in neurons. The primary cultured hippocampal neurons of rat were exposed to the commercial decabromodiphenyl ether (deca-BDE), and the neurite length, bi- furcation, and synapse formation and maturation were evaluated, based on the confocal microscope imaging. The results showed that the development inhibition in neurons occurred at 15 μmol/L, indi- cating that PBDE is a potent neurotoxicant and it might obviously inhibit the development of cultured neurons.展开更多
文摘Background It is a common phenomenon that children experience multiple general anesthesias in clinical practice, which raises the question whether repeated exposure to general anesthetics would interfere with the development of the central nervous system of children. The present study was designed to evaluate the effects of repeated treatment with ketamine or midazolam on postnatal dendrite development by examining the morphology of the dendritic spines of the pyramidal neurons in the hippocampal CA1 region in mice. Methods The transgenic green fluorescent protein-M line （GFP-M） mice were used in this study. Ketamine （100 mg/kg） midazolam （50 mg/kg） or saline （10 ml/kg） was administered intraperitoneally once a day on consecutive days from postnatal day 8 （P8） to postnatal day 12 （P12）. At postnatal day 13 （P13） and postnatal day 30 （P30）, the density and length of the apical dendritic spines of the pyramidal neurons in the hippocampal CA1 region were examined under a confocal microscope. Results At P13, for both the ketamine group and the midazolam group, the dendritic spines were found with a comparatively lower density and longer average length than in the control group. At P30, no significant difference in the density or average length of dendritic spines was found between the anesthetic group and control group. Conclusions This study indicated that repeated exposure to ketamine or midazolam in neonatal mice impaired dendritic spine maturation immediately afterwards, but this influence seemed to disappear during further postnatal development.
基金Supported by the National Basic Research Program of China (Grant No. 2003CB- 415001)the National Natural Science Foundation of China (Grant No. 30321002)the Chinese Academy of Sciences (Grant No. KJCX2-SW-H06)
文摘Polybrominated diphenyl ether (PBDE) is a persistently environmental pollutant ubiquitously found in wildlife and humans. Although concern on PBDE’s toxic effects is steadily increasing, its action on the central nervous system (CNS) remains largely unknown. To address this issue, the present study ex- amined the development inhibition of PBDE in neurons. The primary cultured hippocampal neurons of rat were exposed to the commercial decabromodiphenyl ether (deca-BDE), and the neurite length, bi- furcation, and synapse formation and maturation were evaluated, based on the confocal microscope imaging. The results showed that the development inhibition in neurons occurred at 15 μmol/L, indi- cating that PBDE is a potent neurotoxicant and it might obviously inhibit the development of cultured neurons.
