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Corticosterone increases serotonin type-3 receptor mRNA in rat pheochromocytoma-12 cells.

机译:皮质酮可增加大鼠嗜铬细胞瘤12细胞中3型血清素受体的mRNA。

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摘要

Serotonin type-3 (5-HT3) receptors are cation permeable membrane receptors which are involved in modulation of calcium entry in neuronal cells. Along with other ion-channels such as the N-methyl-D-aspartate receptor, it appears to be a target for the actions of ethanol and has been the focus of considerable work in this regard. Since in animals, ethanol exposure results in elevations of corticosteroids in both acute and chronic conditions, we studied the effects of both ethanol and corticosteroid exposure on 5-HT3 gene expression in an in situ pheochromocytoma-12 (PC12) cell model. We found that ethanol exposure alone (80 mMx4 days) did not significantly alter target gene expression. Corticosterone (CORT) (50, 150, and 300 ng/ml) resulted in significant increases in 5-HT3 expression which were attenuated by mifeprestone (50 ng/ml). Ethanol in combination with CORT did not significantly alter the increase in 5- HT3 mRNA seen with CORT alone. We conclude that in PC12 cells, exposure to CORT at physiologically relevant concentrations increases 5-HT3 gene expression.
机译:3型血清素(5-HT3)受体是阳离子渗透膜受体,参与调节神经元细胞中钙的进入。与其他离子通道(例如N-甲基-D-天冬氨酸受体)一起,它似乎是乙醇作用的目标,并且在这方面一直是大量工作的重点。由于在动物中,乙醇暴露导致急性和慢性条件下皮质类固醇的升高,因此我们在原位嗜铬细胞瘤12(PC12)细胞模型中研究了乙醇和皮质类固醇暴露对5-HT3基因表达的影响。我们发现单独的乙醇暴露(80 mMx4天)不会显着改变靶基因的表达。皮质酮(CORT)(50、150和300 ng / ml)导致5-HT3表达显着增加,但被米非司酮(50 ng / ml)减弱。单独使用CORT的乙醇联合CORT并没有显着改变5-HT3 mRNA的增加。我们得出结论,在PC12细胞中,生理相关浓度的CORT暴露会增加5-HT3基因表达。

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