The tonic model delineating the serotonin transporter polymorphism’s (5-HTTLPR) modulatory effect on anxiety points towards a universal underlying mechanism involving a hyper-or-elevated baseline level of arousal even to non-threatening stimuli. However, to our knowledge, this mechanism has never been observed in non-clinical cohorts exhibiting high anxiety. Moreover, empirical support regarding said association is mixed, potentially because of publication bias with a relatively small sample size. Hence, how the 5-HTTLPR modulates neural correlates remains controversial. Here we show that 5-HTTLPR short-allele carriers had significantly increased baseline ERPs and reduced fearful MMN, phenomena which can nevertheless be reversed by acute anxiolytic treatment. This provides evidence that the 5-HTT affects the automatic processing of threatening and non-threatening voices, impacts broadly on social cognition, and conclusively asserts the heightened baseline arousal level as the universal underlying neural mechanism for anxiety-related susceptibilities, functioning as a spectrum-like distribution from high trait anxiety non-patients to anxiety patients.

描绘5-羟色胺转运蛋白多态性（5-HTTLPR）对焦虑的调节作用的补品模型指向一种普遍的潜在机制，该机制涉及刺激的基线水平升高或升高，甚至刺激到非威胁性刺激。然而，据我们所知，在表现出高度焦虑的非临床人群中从未观察到这种机制。而且，关于所述关联的经验支持是混杂的，这可能是由于相对较小的样本量的出版偏见。因此，5-HTTLPR如何调节神经相关仍存在争议。这里我们显示5-HTTLPR短等位基因携带者的基线ERPs显着增加，而可怕的MMN减少，急性抗焦虑治疗仍然可以逆转这种现象。这提供了证据，表明5-HTT会影响威胁性和非威胁性声音的自动处理，广泛影响社会认知，并最终断言基线唤醒水平的升高是焦虑相关易感性的普遍潜在神经机制，具有频谱作用。特质性焦虑症非患者到焦虑症患者的类似分布。