ArticleMolecular psychiatry2020
AP-1 controls the p11-dependent antidepressant response.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 45 citations in OpenAlex.
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Peripheral blood transcriptomic biomarkers for predicting antidepressant response in major depressive disorder.BMC psychiatry · 2026Article
- Optimization of potential targets for antidepressant Chinese medicines: AI and multi-omics methods.Chinese medicine · 2026Review
- Deciphering the impact of genetic variants on vulnerability to Opioid Use Disorder.Frontiers in cellular neuroscience · 2026Article
- Association of TNF-α polymorphisms rs1800629 (-308G>A) and rs361525 (-238G>A) with type 2 diabetes mellitus in the Punjabi population of Pakistan.Frontiers in endocrinology · 2025Article
- Anti-depression molecular mechanism elucidation of the phytochemicals in edible flower ofFood science & nutrition · 2024Article
- Shared and unique transcriptomic signatures of antidepressant and probiotics action in the mammalian brain.Molecular psychiatry · 2024Article
- Transcriptome-Wide Profiling of Nascent RNA in Neurons with Enriched H3K27ac Signal Elevates eRNA Identification Efficiency.ACS chemical neuroscience · 2024Article
- Quercetin Ameliorates Cognitive Impairment in Depression by Targeting HSP90 to Inhibit NLRP3 Inflammasome Activation.Molecular neurobiology · 2024Article
- Novel Insights into Changes in Gene Expression within the Hypothalamus in Two Asthma Mouse Models: A Transcriptomic Lung-Brain Axis Study.International journal of molecular sciences · 2024Article
- Article
- Brain-Derived Neurotrophic Factor - The Protective Agent Against Neurological Disorders.CNS & neurological disorders drug targets · 2024Article
- Opioid Mechanisms and the Treatment of Depression.Current topics in behavioral neurosciences · 2024Review
- Reduction of p11 in dorsal raphe nucleus serotonergic neurons mediates depression-like behaviors.Translational psychiatry · 2023Article
- Article
- Inhibition of c-Jun in AgRP neurons increases stress-induced anxiety and colitis susceptibility.Communications biology · 2023Article
- Cortical structural differences following repeated ayahuasca use hold molecular signatures.Frontiers in neuroscience · 2023Article
- S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- The opioid system in depression.Neuroscience and biobehavioral reviews · 2022Review
- S100A10 and its binding partners in depression and antidepressant actions.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations dysregulated during depression. To determine their precise mode of action, we tested whether such neuroadaptive processes are modulated by regulation of specific gene expression programs. Here we identify a transcriptional program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selectively activated prior to the onset of the chronic SSRI response. The AP-1 transcriptional program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response. We find that AP-1 function is required for the antidepressant effect in vivo. Furthermore, we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the antidepressant response. Here we put forth a sequential molecular network to track the antidepressant response and provide a new avenue that could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.
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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.