ArticleMolecular psychiatry2015
Alteration by p11 of mGluR5 localization regulates depression-like behaviors.
Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- Systematic identification of p11 as a signaling modulator across the GPCRome.Science advances · 2026Article
- Genetic alterations in SUPT6H are associated with neurodevelopmental disorders.Biochimica et biophysica acta. Molecular basis of disease · 2026Article
- TrkB/mGluR5 cross-talk underlies a synaptic metaplasticity mechanism of ketamine.Science advances · 2026Article
- Loss of mGluMolecular psychiatry · 2024Article
- A proximity proteomics pipeline with improved reproducibility and throughput.Molecular systems biology · 2024Article
- The role of mGluR5 on the therapeutic effects of ketamine in Wistar rats.Psychopharmacology · 2024Article
- A proximity proteomics pipeline with improved reproducibility and throughput.bioRxiv : the preprint server for biology · 2024Article
- Ahnak in the prefrontal cortex mediates behavioral correlates of stress resilience and rapid antidepressant action in mice.Frontiers in molecular neuroscience · 2024Article
- Reduction of p11 in dorsal raphe nucleus serotonergic neurons mediates depression-like behaviors.Translational psychiatry · 2023Article
- Recent Advances in Molecular and Cellular Functions of S100A10.Biomolecules · 2023Review
- Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours by inhibiting ANXA2 degradation.Cellular and molecular life sciences : CMLS · 2023Article
- Role of P11 through serotonergic and glutamatergic pathways in LID.Molecular biology reports · 2023Review
- Saikosaponin D exerts antidepressant effect by regulating Homer1-mGluR5 and mTOR signaling in a rat model of chronic unpredictable mild stress.Chinese medicine · 2022Article
- Update on GPCR-based targets for the development of novel antidepressants.Molecular psychiatry · 2022Review
- S100A10 and its binding partners in depression and antidepressant actions.Frontiers in molecular neuroscience · 2022Review
- Molecular and Cellular Adaptations in Hippocampal Parvalbumin Neurons Mediate Behavioral Responses to Chronic Social Stress.Frontiers in molecular neuroscience · 2022Article
- The Annexin A2/S100A10 Complex: The Mutualistic Symbiosis of Two Distinct Proteins.Biomolecules · 2021Review
- Loss of mGluR5 in D1 Receptor-Expressing Neurons Improves Stress Coping.International journal of molecular sciences · 2021Article
- Hippocampal mossy cell involvement in behavioral and neurogenic responses to chronic antidepressant treatment.Molecular psychiatry · 2020Article
- Systemic immunization with altered myelin basic protein peptide produces sustained antidepressant-like effects.Molecular psychiatry · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Mood disorders and antidepressant therapy involve alterations of monoaminergic and glutamatergic transmission. The protein S100A10 (p11) was identified as a regulator of serotonin receptors, and it has been implicated in the etiology of depression and in mediating the antidepressant actions of selective serotonin reuptake inhibitors. Here we report that p11 can also regulate depression-like behaviors via regulation of a glutamatergic receptor in mice. p11 directly binds to the cytoplasmic tail of metabotropic glutamate receptor 5 (mGluR5). p11 and mGluR5 mutually facilitate their accumulation at the plasma membrane, and p11 increases cell surface availability of the receptor. Whereas p11 overexpression potentiates mGluR5 agonist-induced calcium responses, overexpression of mGluR5 mutant, which does not interact with p11, diminishes the calcium responses in cultured cells. Knockout of mGluR5 or p11 specifically in glutamatergic neurons in mice causes depression-like behaviors. Conversely, knockout of mGluR5 or p11 in GABAergic neurons causes antidepressant-like behaviors. Inhibition of mGluR5 with an antagonist, 2-methyl-6-(phenylethynyl)pyridine (MPEP), induces antidepressant-like behaviors in a p11-dependent manner. Notably, the antidepressant-like action of MPEP is mediated by parvalbumin-positive GABAergic interneurons, resulting in a decrease of inhibitory neuronal firing with a resultant increase of excitatory neuronal firing. These results identify a molecular and cellular basis by which mGluR5 antagonism achieves its antidepressant-like activity.
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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.