Increased Signaling via Adenosine A1 Receptors, Sleep Deprivation, Imipramine, and Ketamine Inhibit Depressive-like Behavior via Induction of Homer1a
Open accessAbstract
Major depressive disorder is among the most commonly diagnosed disabling mental diseases. Several non-pharmacological treatments of depression upregulate adenosine concentration and/or adenosine A1 receptors (A1R) in the brain. To test whether enhanced A1R signaling mediates antidepressant effects, we generated a transgenic mouse with enhanced doxycycline-regulated A1R expression, specifically in forebrain neurons. Upregulating A1R led to pronounced acute and chronic resilience toward depressive-like behavior in various tests. Conversely, A1R knockout mice displayed an increased depressive-like behavior and were resistant to the antidepressant effects of sleep deprivation (SD). Various antidepressant treatments increase homer1a expression in medial prefrontal cortex (mPFC). Specific siRNA knockdown of homer1a in mPFC enhanced depressive-like behavior and prevented the antidepressant effects of A1R upregulation, SD, imipramine, and ketamine treatment. In contrast, viral overexpression of homer1a in the mPFC had antidepressant effects. Thus, increased expression of homer1a is a final common pathway mediating the antidepressant effects of different antidepressant treatments.
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Neuronal A1 receptors exhibit hypofunction caused by a decrease in astrocyte-derived adenosine levels; this decrease, as well as depressive-like behavior, can be reversed by certain antidepressants.
“Additionally, neuronal A1 receptors exhibit hypofunction caused by a decrease in astrocyte-derived adenosine levels; 103 this decrease, as well as depressive-like behavior, can be reversed by certain antidepressants. 104 , 105”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [105]
The Results (‘Behavioral Effects of A1R Deletion’; page unavailable) report that imipramine improved depressive-like behavior in mice. The Discussion links astrocyte-released adenosine to neuronal A1 receptors, but the paper does not report that antidepressants reverse a decrease in astrocyte-derived adenosine levels. The first clause is separately cited to reference 103; the unsupported part of the clause attributed here is the claimed reversal of adenosine levels. (LLM, conf=0.85)
Experimental — accuracy not yet measuredPSD proteins (e.g., Homers, Norbin) may be involved in the response or lack of sustained response to canonical antidepressants, as well as ketamine and other NMDA receptor antagonists.
“Multiple lines of evidence both a preclinical and clinical level, suggest that PSD proteins (i.e. Homers, Norbin) may be involved in the response or lack of (sustained) response to canonical antidepressant [59, 60], as well as ketamine and other NMDAreceptor antagonists [61, 62].”
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- Authors
- Serchov, T., Clement, H.-W., Schwarz, M. K., Iasevoli, F., Tosh, D. K., Idzko, M., Jacobson, K. A., de Bartolomeis, A., Normann, C., Biber, K., & van Calker, D.
- Affiliations
- University Medical Center Freiburg (DE)
- University of Bonn (DE)
- Federico II University Hospital (IT)
- National Institutes of Health (US)
- University Medical Center Groningen (NL)
- Corresponding author
- Biber, Knut
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 87
- Issue
- 3
- Pages
- 549-562
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4803038
- OpenAlex
- W1903124221
- Cited by
- 210
- References
- 63
- Citations by year
- 2026: 10 · 2025: 21 · 2024: 17 · 2023: 19 · 2022: 22 · 2021: 23 · 2020: 23 · 2019: 24 · 2018: 15 · 2017: 23 · 2016: 7 · 2015: 5
- FWCI
- 12.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- Funders
- European Commission
- Deutsche Forschungsgemeinschaft (CA 115/5-4)
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (ZIADK031117)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- adenosine A1 receptor, Homer1a, depression, antidepressant effects, sleep deprivation, imipramine, ketamine, medial prefrontal cortex, depression-like behavior, siRNA knockdown, viral overexpression
- MeSH terms
- Homer Scaffolding Proteins, Animals, Carrier Proteins, Depression, Humans, Imipramine, Ketamine, Mice, Transgenic, Sleep Deprivation, Signal Transduction, Prefrontal Cortex, Mice, Knockout, Receptor, Adenosine A1, Mice, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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