ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2019
Homeostatic cAMP regulation by the RGS7 complex controls depression-related behaviors.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Non-Ceruloplasmin Copper Identifies a Subtype of Alzheimer's Disease (CuAD): Characterization of the Cognitive Profile and Case of a CuAD Patient Carrying anInternational journal of molecular sciences · 2023Pooled it
- The role of ucOCN in aerobic exercise induced amelioration of autism spectrum disorder phenotypes.iScience · 2026Article
- Targeting mGlyR with nanobodies for depression.Nature communications · 2026Article
- Bmal1 Modulates Striatal cAMP Signaling and Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The G protein modifier KCTD5 tunes the decoding of neuromodulatory signals necessary for motor function in striatal neurons.PLoS biology · 2025Article
- Cryo-EM structure of human class C orphan GPCR GPR179 involved in visual processing.Nature communications · 2024Article
- Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens.Cellular and molecular life sciences : CMLS · 2024Article
- Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR.Science (New York, N.Y.) · 2023Article
- Expression Mapping and Functional Analysis of Orphan G-Protein-Coupled Receptor GPR158 in the Adult Mouse Brain Using a GPR158 Transgenic Mouse.Biomolecules · 2023Article
- Review
- Novel Molecular Targets of Antidepressants.Molecules (Basel, Switzerland) · 2022Review
- Cryo-EM structure of human GPR158 receptor coupled to the RGS7-Gβ5 signaling complex.Science (New York, N.Y.) · 2022Article
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- Structure of the class C orphan GPCR GPR158 in complex with RGS7-Gβ5.Nature communications · 2021Article
- Gαo is a major determinant of cAMP signaling in the pathophysiology of movement disorders.Cell reports · 2021Article
- Review
- Beyond the Ligand: Extracellular and Transcellular G Protein-Coupled Receptor Complexes in Physiology and Pharmacology.Pharmacological reviews · 2019Review
- The signaling proteins GPR158 and RGS7 modulate excitability of L2/3 pyramidal neurons and control A-type potassium channel in the prelimbic cortex.The Journal of biological chemistry · 2019Article
- Article
- rs12411980 single-nucleotide polymorphism related toMolecular painArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Affective disorders arise from abnormal responses of the brain to prolonged exposure to challenging environmental stimuli. Recent work identified the orphan receptor GPR158 as a molecular link between chronic stress and depression. Here we reveal a non-canonical mechanism by which GPR158 exerts its effects on stress-induced depression by the complex formation with Regulator of G protein Signaling 7 (RGS7). Chronic stress promotes membrane recruitment of RGS7 via GPR158 in the medial prefrontal cortex (mPFC). The resultant complex suppresses homeostatic regulation of cAMP by inhibitory GPCRs in the region. Accordingly, RGS7 loss in mice induces an antidepressant-like phenotype and resiliency to stress, whereas its restoration within the mPFC is sufficient to rescue this phenotype in a GPR158-dependent way. These findings mechanistically link the unusual orphan receptor-RGS complex to a major stress mediator, the cAMP system and suggest new avenues for pharmacological interventions in affective disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.