Transcriptional Dys-regulation in Anxiety and Major Depression: 5-HT1A Gene Promoter Architecture as a Therapeutic Opportunity

Albert, Paul; Fiori, Laura

doi:10.2174/13816128113196660740

Cited by 46Neurotransmitter Receptor Influence on BehaviorTreatment of Major DepressionNeuroscience and Neuropharmacology Research

Transcriptional Dys-regulation in Anxiety and Major Depression: 5-HT1A Gene Promoter Architecture as a Therapeutic Opportunity

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Albert, Paul, Fiori, Laura·2014·Current Pharmaceutical Design

DOI 10.2174/13816128113196660740PMC PMC4514528

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Abstract

The etiology of major depression remains unclear, but reduced activity of the serotonin (5-HT) system remains implicated and treatments that increase 5-HT neurotransmission can ameliorate depressive symptoms. 5-HT1A receptors are critical regulators of the 5- HT system. They are expressed as both presynaptic autoreceptors that negatively regulate 5-HT neurons, and as post-synaptic heteroreceptors on non-serotonergic neurons in the hippocampus, cortex, and limbic system that are critical to mediate the antidepressant actions of 5-HT. Thus, 5-HT1A auto- and heteroreceptors have opposite actions on serotonergic neurotransmission. Because most 5-HT1A ligands target both auto- and heteroreceptors their efficacy has been limited, resulting in weak or unclear responses. We propose that by understanding the transcriptional regulation of the 5-HT1A receptor it may be possible to regulate its expression differentially in raphe and projection regions. Here we review the transcriptional architecture of the 5-HT1A gene (HTR1A) with a focus on specific DNA elements and transcription factors that have been shown to regulate 5-HT1A receptor expression in the brain. Association studies with the functional HTR1A promoter polymorphism rs6295 suggest a new model for the role of the 5-HT1A receptor in susceptibility to depression involving early deficits in cognitive, fear and stress reactivity as stressors that may ultimately lead to depression. We present evidence that by targeting specific transcription factors it may be possible to oppositely regulate 5-HT1A auto- and heteroreceptor expression, synergistically increasing serotonergic neurotransmission for the treatment of depression.

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Up-regulated serotonin 1A receptors may result from a 5-HT1A gene promoter polymorphism that causes overexpression of autoreceptors.
“Up-regulated serotonin 1A receptors may result from a 5-HT1A gene promoter polymorphism that causes overexpression of autoreceptors as a result of less binding of inhibitory transcription factors in serotonin neurons (120, 121).”
From A brain-centric model of suicidal behavior (2020) · cites this paper as [121]

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Authors: Albert, P., & Fiori, L.
Affiliations: Bentham Science Publishers (United Arab Emirates) (AE)
University of Ottawa (CA)
ORCID: Albert, Paul
Fiori, Laura
Venue: Current Pharmaceutical Design
Publisher: Bentham Science Publishers Ltd.
Published: 2014-06
Volume: 20
Issue: 23
Pages: 3738-3750
ISSN: 1381-6128 (ISSN-L)
DOI: 10.2174/13816128113196660740
PMC: PMC4514528
OpenAlex: W2042244259
Cited by: 46
References: 160
Citations by year: 2026: 3 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 7 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 1 · 2015: 2
FWCI: 1.22
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Current Pharmaceutical Design (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Canadian Institutes of Health Research (115098_1)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: 5-HT1A receptor, transcriptional regulation, promoter, major depressive disorder, anxiety, serotonergic system, autoreceptors, heteroreceptors, transcription factors, genetic susceptibility to depression, stress reactivity, cognitive impairment, fear, antidepressant targets, serotonergic neurotransmission
MeSH terms: Animals, Anxiety, Base Sequence, Major Depressive Disorder, Disease Models, Animal, Gene Expression Regulation, Gene Frequency, Humans, Molecular Sequence Data, Promoter Regions, Genetic, Species Specificity, Transcription, Genetic, Sequence Alignment, Receptor, Serotonin, 5-HT1A, Regulatory Elements, Transcriptional, Gene-Environment Interaction

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Transcriptional Dys-regulation in Anxiety and Major Depression: 5-HT1A Gene Promoter Architecture as a Therapeutic Opportunity

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