ArticleCommunications biology2020
An integrative analysis of 5HTT-mediated mechanism of hyperactivity to non-threatening voices.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Negative emotionality downregulation affects moral choice but not moral judgement of harm: a pharmacological study.Scientific reports · 2024Article
- Application and Mechanisms of Internet-Based Cognitive Behavioral Therapy (iCBT) in Improving Psychological State in Cancer Patients.Journal of Cancer · 2023Review
- Interaction effects of the 5-HTT and MAOA-uVNTR gene variants on pre-attentive EEG activity in response to threatening voices.Communications biology · 2022Article
- The Multifaceted Effects of Serotonin Transporter Polymorphism (5-HTTLPR) on Anxiety, Implicit Moral Attitudes, and Harmful Behaviors.Frontiers in psychology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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