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Neurotoxicity of prenatal alcohol exposure on medullary pre-B?tzinger complex neurons in neonatal rats

Neural Regeneration Research 2015年第7期10卷 1095-1100页

作者： Ming-li Ji Yun-hong Wu Zhi-bin Qian Department of Physiology Xinxiang Medical University Department of Functional Laboratory Xinxiang Medical University

prenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is unknown whether the 5-hydroxytryptamine 2A receptor（5-HT2AR） is involved in the effects of prenatal alcohol exposure. In the present study, pregnant female rats received drinking water containing alcohol at concentrations of 0%, 1%, 2%, 4%, 8% or 10%（v/v） throughout the gestation period. Slices of the medulla from 2-day-old neonatal rats were obtained to record respiratory rhythmical discharge activity. 5-HT2 AR protein and m RNA levels in the pre-B？tzinger complex of the respiratory center were measured by western blot analysis and quantitative RT-PCR, respectively. Compared with the 0% alcohol group, respiratory rhythmical discharge activity in medullary slices in the 4%, 8% and 10% alcohol groups was decreased, and the reduction was greatest in the 8% alcohol group. Respiratory rhythmical discharge activity in the 10% alcohol group was irregular. Thus, 8% was the most effective alcohol concentration at attenuating respiratory rhythmical discharge activity. These findings suggest that prenatal alcohol exposure attenuates respiratory rhythmical discharge activity in neonatal rats by downregulating 5-HT2 AR protein and m RNA levels.

关键词： nerve regeneration brain injury prenatal alcohol exposure pre-B?tzinger complex respiratory depression neonatal rats medullary slice medullary respiratory center respiratory rhythmical discharge activity respiratory neuron 5-hydroxytryptamine 2A receptor neural regeneration

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Ceramide is involved in alcohol-induced neural proliferation

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Neural Regeneration Research 2013年第23期8卷 2178-2189页

作者： Zhixin Wang Tongxing Deng Jiexin Deng Jinbo Deng Xiaoqun Gao Yuanyuan Shi Bin Liu Zhanyou Ma Haixiao Jin Institute of Neurobiology Henan University Department of Anatomy Basic Medical CollegeZhengzhou University Department of Anatomy Luohe Medical College

prenatal alcohol exposure, especially during early pregnancy, can lead to fetal alcohol syndrome. The pharmacological and toxicological mechanisms of ethanol are related to the effects of ceramide In this study, we established an alcohol exposure model in wild-type mice and in knockout mice for the key enzyme involved in ceramide metabolism, sphingomyelin synthase 2. This model received daily intragastric administration of 25% ethanol, and pups were used at postnatal days 0, 7, 14, 30 for experiments. Serology and immunofluorescence staining found that ethanol exposure dose-dependently reduced blood sphingomyelin levels in two genotypes of pups, and increased neural cell proliferation and the number of new neurons in the hippocampal dentate gyrus. Western blot analysis showed that the relative expression level of protein kinase C e increased in two genotypes of pups after ethanol exposure. Compared with witd-type pups, the expression level of the important activator protein of the ceramide/ceramide-l-phosphate pathway, protein kinase C a, was reduced in the hippocampus of sphingomyelin synthase 2 knockouts. Our findings illustrate that ceramide is involved in alcohol-induced neural proliferation in the hippocampal dentate gyrus of pups after prenatal ethanol exposure, and the mechanism may be associated with increased ex- pression of protein kinase C a activating the ceramide/ceramide-l-phosphate pathway.

关键词： neural regeneration brain injury ceramide neural cells proliferation prenatal alcohol exposure sphingomyelin synthase 2 knockout mice sphingomyelin sphingomyelin synthase cera-mide-l-phosphate fetal alcohol syndrome grants-supported paper neuroregeneration

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