The DOI matches its Crossref record; 139 of the 139 references it cites were found in a registry or an index.
Serotonin-prefrontal cortical circuitry in anxiety and depression phenotypes: pivotal role of pre- and post-synaptic 5-HT1A receptor expression
Open accessAbstract
Decreased serotonergic activity has been implicated in anxiety and major depression, and antidepressants directly or indirectly increase the long-term activity of the serotonin system. A key component of serotonin circuitry is the 5-HT1A autoreceptor, which functions as the major somatodendritic autoreceptor to negatively regulate the "gain" of the serotonin system. In addition, 5-HT1A heteroreceptors are abundantly expressed post-synaptically in the prefrontal cortex (PFC), amygdala, and hippocampus to mediate serotonin actions on fear, anxiety, stress, and cognition. Importantly, in the PFC 5-HT1A heteroreceptors are expressed on at least two antagonist neuronal populations: excitatory pyramidal neurons and inhibitory interneurons. Rodent models implicate the 5-HT1A receptor in anxiety- and depression-like phenotypes with distinct roles for pre- and post-synaptic 5-HT1A receptors. In this review, we present a model of serotonin-PFC circuitry that integrates evidence from mouse genetic models of anxiety and depression involving knockout, suppression, over-expression, or mutation of genes of the serotonin system including 5-HT1A receptors. The model postulates that behavioral phenotype shifts as serotonin activity increases from none (depressed/aggressive not anxious) to low (anxious/depressed) to high (anxious, not depressed). We identify a set of conserved transcription factors including Deaf1, Freud-1/CC2D1A, Freud-2/CC2D1B and glucocorticoid receptors that may confer deleterious regional changes in 5-HT1A receptors in depression, and how future treatments could target these mechanisms. Further studies to specifically test the roles and regulation of pyramidal vs. interneuronal populations of 5-HT receptors are needed better understand the role of serotonin in anxiety and depression and to devise more effective targeted therapeutic approaches.
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“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 [120]
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Metadata
- Authors
- Albert, P. R., Vahid-Ansari, F., & Luckhart, C.
- Affiliations
- University of Ottawa (CA)
- Corresponding author
- Albert, Paul R.
- Venue
- Frontiers in Behavioral Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2014-06-06
- Volume
- 8
- Pages
- 199-199
- ISSN
- 1662-5153 (ISSN-L)
- PMC
- PMC4047678
- OpenAlex
- W2092933199
- Cited by
- 321
- References
- 139
- Citations by year
- 2026: 27 · 2025: 31 · 2024: 27 · 2023: 24 · 2022: 24 · 2021: 21 · 2020: 24 · 2019: 27 · 2018: 30 · 2017: 33 · 2016: 19 · 2015: 26 · 2014: 8
- FWCI
- 3.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Behavioral Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Canadian Institutes of Health Research (123426_1, 115098_1)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- serotonin, 5-HT1A receptor, prefrontal cortex, anxiety, depression, autoreceptors, heteroreceptors, pyramidal neurons, interneurons, DEAF1, glucocorticoid receptor, genetic mouse models, antidepressant targets
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