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Serotonin (5-HT) release and uptake measured by real-time electrochemical techniques in the rat ileum

机译:通过实时电化学技术测量大鼠回肠中5-羟色胺(5-HT)的释放和摄取

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Serotonin (5-HT)release and uptake measured by real-time electrochemical tech-niques in the rat ileum. Am J Physiol Gastrointest Liver Phys-iol 295: G1228-G1236, 2008. First published October 16, 2008; -Serotonin (5-HT) is released from the enterochromaffin cells and plays an important role in regulating intestinal function. Although the release of 5-HT is well documented, the contribution of the serotonin reuptake transporter (SERT) to the levels and actions of 5-HT in the intestine is unclear. This study aimed to demonstrate real-time SERT activity in ileal mucosa and to assess the effects of SERT inhibition using fluoxetine. Electrochemical recordings were made from the mucosa in full-thickness preparations of rat ileum using a carbon fiber electrode to measure 5-HT oxidation current and a force transducer to record circular muscle (CM) tension. Compression of the mucosa stimulated a peak 5-HT release of 12 +-6 muM, which decayed to 7 +- ,4 muM Blockade of SERT with fluoxetine (1 muM) increased the peak compression-evoked release to 19+- 9 muM, and the background levels of 5-HT increased to 11 +-7 muM (P < 0.05, n = 7). When 5-HT was exogenously applied to the mucosa, fluoxetine caused a significant increase in the time to 50% and 80% decay of the oxidation current. Fluoxetine also increased the spontaneous CM motility (P < 0.05; n = 1) but did not increase the CM contraction-evoked 5-HT release (P > 0.05, n = 5). In conclu-sion, this is the first characterization of the real-time uptake of 5-HT into the rat intestine. These data suggest that SERT plays an important role in the modulation of 5-HT concentrations that reach intestinal 5-HT receptors.
机译:通过实时电化学技术在大鼠回肠中测量5-羟色胺(5-HT)的释放和摄取。 Am J胃肠胃肠道疾病295:G1228-G1236,2008年。2008年10月16日首次发布; -5-羟色胺(5-HT)从肠嗜铬细胞释放,并在调节肠道功能中起重要作用。尽管5-HT的释放有充分的文献记载,但5-羟色胺再摄取转运蛋白(SERT)对肠道中5-HT的水平和作用的贡献尚不清楚。这项研究旨在证明回肠粘膜中的实时SERT活性,并评估氟西汀对SERT抑制的影响。使用碳纤维电极测量5-HT氧化电流并用力传感器记录环形肌肉(CM)张力,从大鼠回肠全层制剂中的粘膜进行电化学记录。粘膜压迫刺激了5-HT峰值释放为12 + -6μM,衰减至7 +-,4μM用氟西汀(1μM)阻断了SERT,从而将压迫诱发峰释放为19 +-9μM, 5-HT的背景水平增加到11 + -7μM(P <0.05,n = 7)。当将5-HT外源施加到粘膜上时,氟西汀在时间上显着增加,使氧化电流衰减了50%和80%。氟西汀还增加了自发性CM运动(P <0.05; n = 1),但没有增加CM收缩引起的5-HT释放(P> 0.05,n = 5)。结论是,这是5-HT实时摄入大鼠肠道的第一个特征。这些数据表明,SERT在调节到达肠道5-HT受体的5-HT浓度中起重要作用。

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