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Phenelzine treatment increases transcription factor AP-2 levels in rat brain

机译:苯乙嗪治疗可增加大鼠脑中转录因子AP-2的水平

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摘要

BackgroundThe elevations of noradrenaline (NA) and serotonin (5-HT) levels in response to acute serotonin reuptake inhibitor (SSRI) or tricyclic antidepressant (TCA) exposure are not consistent with the time course for the therapeutic action of these antidepressants. Thus, neuronal adaptations are needed for the therapeutic effect to arise. Transcription factor Activating Protein –2 (AP-2) is critical for mammalian neural gene expression. Several genes involved in brainstem CNS transmitter systems, especially the monoamines, have AP-2 binding sites in their regulatory regions. We have previously shown that treatment with citalopram and imipramin resulted in a decrease in AP-2α and AP-2β levels in rat brain. We have also reported an association between a specific genotype of AP-2β to personality traits, binge-eating disorder and platelet monoamine oxidase (MAO) activity.
机译:背景对急性5-羟色胺再摄取抑制剂(SSRI)或三环抗抑郁药(TCA)暴露的响应,去甲肾上腺素(NA)和5-羟色胺(5-HT)的水平升高与这些抗抑郁药的治疗作用的时程不一致。因此,需要神经元适应以产生治疗效果。转录因子激活蛋白-2(AP-2)对于哺乳动物神经基因表达至关重要。脑干中枢神经系统递质系统中涉及的几个基因,尤其是单胺,在其调控区域具有AP-2结合位点。先前我们已经证明,用西酞普兰和伊米拉明治疗可导致大鼠脑内AP-2α和AP-2β水平降低。我们还报道了AP-2β特定基因型与人格特质,暴饮暴食症和血小板单胺氧化酶(MAO)活性之间的关联。

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