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Cited by 489Treatment of Major DepressionNeurotransmitter Receptor Influence on BehaviorTryptophan and brain disorders

The DOI matches its Crossref record; 190 of the 190 references it cites were found in a registry or an index.

The role of 5-HT receptors in depression

Open access
Yohn, Christine N., Gergues, Mark M., Samuels, Benjamin Adam·2017·Molecular Brain
DOI 10.1186/s13041-017-0306-yPMC PMC5483313
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Abstract

Depression is a polygenic and highly complex psychiatric disorder that remains a major burden on society. Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), are some of the most commonly prescribed drugs worldwide. In this review, we will discuss the evidence that links serotonin and serotonin receptors to the etiology of depression and the mechanisms underlying response to antidepressant treatment. We will then revisit the role of serotonin in three distinct hypotheses that have been proposed over the last several decades to explain the pathophysiology of depression: the monoamine, neurotrophic, and neurogenic hypotheses. Finally, we will discuss how recent studies into serotonin receptors have implicated specific neural circuitry in mediating the antidepressant response, with a focus being placed on the hippocampus.

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Crossref · 10.1186/s13041-017-0306-y

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Figures

Fig. 1 A proposed model of the hippocampal microcircuit underlying the effects of increased serotonin on the dentate gyrus. First, chronic SSRI administration increases 5-HT levels, which results in activation of 5-HTRs on dentate gyrus granule cells. Activation of 5HT-1ARs on mature granular cells ultimately results in release of downstream growth factors such as BDNF, VEGF, and others, which bind to receptors on neural precursor cells (NPCs) in the subgranular zone. NPCs then proliferate and differentiate into young adult born granule cells (abGCs), which will begin to migrate, mature, and finally integrate into the granule cell layer. However, the young abGCs have distinct plasticity properties from the mature dentate gyrus granule cells and activate local GABAergic interneurons to evoke strong inhibitory input to the mature granule cells
Fig. 1 A proposed model of the hippocampal microcircuit underlying the effects of increased serotonin on the dentate gyrus. First, chronic SSRI administration increases 5-HT levels, which results in activation of 5-HTRs on dentate gyrus granule cells. Activation of 5HT-1ARs on mature granular cells ultimately results in release of downstream growth factors such as BDNF, VEGF, and others, which bind to receptors on neural precursor cells (NPCs) in the subgranular zone. NPCs then proliferate and differentiate into young adult born granule cells (abGCs), which will begin to migrate, mature, and finally integrate into the granule cell layer. However, the young abGCs have distinct plasticity properties from the mature dentate gyrus granule cells and activate local GABAergic interneurons to evoke strong inhibitory input to the mature granule cellsCC BY · PubMed Central
Fig. 2 The expression of 5-HT1A receptors along the dorsoventral axis of the hippocampus in a rodent brain. 5-HT1AR expression is highest in dorsal CA1 and ventral dentate gyrus. The dorsal and ventral hippocampus participate in distinct circuitry, with the ventral hippocampus projecting to limbic structures. Therefore, 5-HT1ARs on dentate gyrus granule cells are well positioned to exert an influence on mood related behaviors
Fig. 2 The expression of 5-HT1A receptors along the dorsoventral axis of the hippocampus in a rodent brain. 5-HT1AR expression is highest in dorsal CA1 and ventral dentate gyrus. The dorsal and ventral hippocampus participate in distinct circuitry, with the ventral hippocampus projecting to limbic structures. Therefore, 5-HT1ARs on dentate gyrus granule cells are well positioned to exert an influence on mood related behaviorsCC BY · PubMed Central

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Citations

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Research works printed but not linked: 1

  1. Feighner JP, Boyer WF. Selective serotonin reuptake inhibitors, 2nd edition: advances in basic research and clinical practice. Chichester: Wiley; 1996.

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Metadata

Authors
Yohn, C. N., Gergues, M. M., & Samuels, B. A.
Affiliations
Rutgers, The State University of New Jersey (US)
Corresponding author
Samuels, Benjamin Adam
ORCID
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2017-06-24
Volume
10
Issue
1
Pages
28-28
ISSN
1756-6606 (ISSN-L)
DOI
10.1186/s13041-017-0306-y
PMC
PMC5483313
OpenAlex
W2695471189
Cited by
485
References
190
Citations by year
2026: 28 · 2025: 53 · 2024: 69 · 2023: 72 · 2022: 60 · 2021: 75 · 2020: 59 · 2019: 38 · 2018: 26 · 2017: 5
FWCI
4.44
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Brain (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Rutgers University Community Repository (Rutgers University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Brain and Behavior Research Foundation (NARSAD Young Investigator)
  • National Institute of Mental Health (R01 MH112861)
Topics
  • Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
depression, serotonin receptors, serotonin, selective serotonin reuptake inhibitors, antidepressant response, monoamine hypothesis, neurotrophic hypothesis, hippocampus, neural circuits, depression pathophysiology
MeSH terms
Animals, Depression, Hippocampus, Humans, Models, Biological, Receptors, Serotonin, Serotonin, Neurogenesis

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