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Dehydroepiandrosterone sulfate (DHEAS) suppresses P2X purinoceptor-coupled responses in PC12 cells.

机译:硫酸脱氢表雄酮(DHEAS)抑制PC12细胞中的P2X嘌呤受体偶联反应。

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摘要

Some steroids rapidly alter neuronal excitability through interaction with neurotransmitter-gated ion channels in addition to their well-known genomic effects via intracellular steroid receptors. Such effects were found in GABA receptor, nicotinic receptors, yet not investigated in P2X purinoceptors. In this study, the effects of dehydroepiandrosterone sulfate on the P2 purinoceptor was investigated. Results show that dehydroepiandrosterone sulfate acutely inhibits P2X purinoceptor functions in PC12 cells. Dehydroepiandrosterone sulfate suppressed ATP-induced cytosolic free calcium concentration ([Ca(2+)](i)) rise, cytosolic free sodium concentration ([Na(+)](i)) rise, and dopamine secretion in the presence of external calcium, but had no effect on ATP-induced [Ca(2+)](i) rise in the absence of external calcium or on UTP-induced [Ca(2+)](i) rise in the absence or presence of external calcium. Our data show that dehydroepiandrosterone sulfate exerted its effect on P2X, but not on the P2Y purinoceptors found in PC12 cells. Estradiol and estrone have similar effects on P2X purinoceptor, but dehydroepiandrosterone and progesterone do not.
机译:一些类固醇除了通过细胞内类固醇受体的众所周知的基因组作用外,还通过与神经递质门控离子通道的相互作用迅速改变了神经元的兴奋性。在GABA受体,烟碱受体中发现了这种作用,但在P2X嘌呤受体中尚未进行研究。在这项研究中,研究了硫酸脱氢表雄酮对P2嘌呤受体的影响。结果表明,硫酸脱氢表雄酮能急性抑制PC12细胞中的P2X嘌呤受体功能。硫酸脱氢表雄酮硫酸盐抑制ATP诱导的胞质游离钙浓度([Ca(2 +)](i))升高,胞质游离钠浓度([Na(+)](i))升高以及在存在外部钙的情况下多巴胺的分泌,但是在没有外部钙的情况下对ATP诱导的[Ca(2 +)](i)升高没有影响,或者在没有外部钙的情况下对UTP诱导的[Ca(2 +)](i)升高没有影响。我们的数据表明,脱氢表雄酮硫酸盐对P2X起作用,但对PC12细胞中发现的P2Y嘌呤受体没有作用。雌二醇和雌酮对P2X嘌呤受体的作用相似,而脱氢表雄酮和孕酮则没有。

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