MiR-16 Targets the Serotonin Transporter: A New Facet for Adaptive Responses to Antidepressants
Abstract
MicroRNA-16 and Depression: Signal transmission between neurons is effected by neurotransmitters such as serotonin. Membrane-bound transporters remove excess neurotransmitters. Disruption of the delicate balance between neurotransmitter release and removal can lead to larger disruptions in neuronal circuitry. Depression and anxiety may be linked to dysfunction of some of these circuits. Uptake inhibitors can be used to treat depression, but the molecular pathways affected have been unclear. Baudry et al. (p. 1537 ) now show that microRNA-16 controls synthesis of the serotonin transporter and that the amount of microRNA-16 can be controlled by the same uptake inhibitors used to treat depression.
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Fluoxetine upregulated the expression of miR-16 in the raphe nucleus of mouse.
“Fluoxetine upregulated the expression of miR-16 in the raphe nucleus of mouse,330”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [330]
Citalopram increased miRNA-16 in mouse brains and decreased SERT protein levels, while exerting antidepressant effects.
“Citalopram increased miRNA-16 in mouse brains and decreased SERT protein levels, while exerting antidepressant effects.330”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [330]
Environmental stress and antidepressant medications change miRNA expression levels in various brain regions that control mood, including the prefrontal cortex, amygdala, nucleus accumbens, locus coeruleus, and dorsal raphe nucleus.
“Environmental stress and antidepressant medications change miRNA expression levels in various brain regions that control mood, including the PFC, amygdala, nucleus accumbens, locus coeruleus, and dorsal raphe nucleus.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [145]
Fluoxetine downregulated miR-16 expression in the locus coeruleus, and blocking miR-16 in this region inhibited depression-like behavior due to chronic stress by altering serotonin transporter expression.
“Fluoxetine downregulated miR-16 expression in the locus coeruleus, and blocking miR-16 in this region inhibited depression-like behavior due to chronic stress by altering serotonin transporter expression.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [145]
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- Authors
- Baudry, A., Mouillet-Richard, S., Schneider, B., Launay, J.-M., & Kellermann, O.
- Affiliations
- Inserm (FR)
- Cellules Souches, Signalisation et Prions, INSERM U747, Université Paris Descartes, 75006 Paris, France.
- F. Hoffmann-La Roche AG (CH)
- Corresponding author
- Launay, Jean-Marie
- Kellermann, Odile
- Venue
- Science
- Published
- 2010-09-17
- Volume
- 329
- Issue
- 5998
- Pages
- 1537-1541
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2060033529
- Cited by
- 480
- References
- 20
- Citations by year
- 2026: 5 · 2025: 16 · 2024: 20 · 2023: 29 · 2022: 26 · 2021: 39 · 2020: 24 · 2019: 26 · 2018: 38 · 2017: 37 · 2016: 40 · 2015: 43 · 2014: 33 · 2013: 36 · 2012: 38
- FWCI
- 24.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- miR-16, serotonin transporter, selective serotonin reuptake inhibitors, fluoxetine, antidepressant response, noradrenergic neurons, serotonergic neurons, locus coeruleus, raphe nuclei, S100β, monoaminergic neurons
- MeSH terms
- Animals, Cell Line, Depression, Fluoxetine, HeLa Cells, Humans, Locus Coeruleus, Nerve Growth Factors, S100 Proteins, Neurons, Norepinephrine, Raphe Nuclei, Serotonin, Protein Biosynthesis, Up-Regulation, Selective Serotonin Reuptake Inhibitors, Antidepressive Agents, Second-Generation, 3' Untranslated Regions, MicroRNAs, Serotonin Plasma Membrane Transport Proteins, Mice, S100 Calcium Binding Protein beta Subunit
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