Role of Fto on CaMKII/CREB signaling pathway of hippocampus in depressive-like behaviors induced by chronic restraint stress mice
Abstract
Background Major depressive disorders (MDD) is one of the most common mental illness in the world. Recently, brain m 6 A /m (fat mass- and obesity-associated gene Fto) was found that exerted an important role in regulating gene expression involved in stress related depression. However, the potential mechanism of Fto on depression still remains elusive. This study investigated the role of Fto and its downstream signaling pathway in hippocampus on chronic restraint stress induced depressive-like behaviors.Methods C57BL/6 mice weighing 20-22 g were randomly divided into 4 groups (Control, Control + Fto-ov, Stress, Stress + Fto-ov). Mice were exposed to chronic restraint stress for 3 consecutive weeks to induce depression model. Mice in the Fto-ov groups were stereotaxic injected with Recombinant Adeno-associated Virus lentivirus (Fto) in hippocampus followed by stress procedure. Depressive-like behaviors were detected after stress procedure. Western blot was used to test hippocampal Fto, p-CaMKII and p-CREB expression. Post synaptic density protein 95 (PSD95) and synaptophysin levels were detected by PCR. Golgi-Cox staining was used to appraise dendritic spine density and branches. Synaptic morphology in hippocampus was determined by electron microscopy.Results We demonstrated that chronic restraint stress induced depressive-like behaviors, decreased protein expression of Fto, p-CaMKII and p-CREB, reduced levels of synaptic plasticity markers (synaptophysin and PSD95) in hippocampus. Moreover, chronic restraint stress led to synaptic morphology alterations (reduced dendritic spine density and number of branches; thinned postsynaptic density). However, these molecules changes and morphology alterations were reversed by stereotaxic injected recombinant adeno-associated Fto-overexpression virus in hippocampus.Conclusions This study found that the modulation of Fto on CaMKII/CREB signaling pathway plays a key role in hippocampal synaptic plasticity, and then ameliorated chronic restraint stress induced depressive-like behaviors.
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Activation of FTO in the hippocampus relieves depression-like behaviors and reduces the density of dendritic spines and the number of branches in mice induced by chronic restraint stress, improving synaptic plasticity.
“Moreover, activation of FTO in the hippocampus relieves depression-like behaviors and reduces the density of dendritic spines and the number of branches in mice induced by chronic restraint stress, improving the synaptic plasticity.373”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [373]
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- Authors
- Shen, J., Yang, L., & Wei, W.
- Affiliations
- Fudan University (CN)
- Corresponding author
- Wei, Wenshi
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2021-05
- Volume
- 406
- Pages
- 113227
- ISSN
- 0166-4328 (ISSN-L)
- OpenAlex
- W3135799194
- Cited by
- 56
- References
- 34
- Citations by year
- 2026: 10 · 2025: 6 · 2024: 9 · 2023: 15 · 2022: 14 · 2021: 2
- FWCI
- 5.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- FTO, chronic restraint stress, depression, hippocampus, synaptic plasticity, dendritic spine density, PSD-95, synaptophysin, postsynaptic density, depression-like behavior
- MeSH terms
- Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Animals, Behavior, Animal, Depression, Disease Models, Animal, Hippocampus, Male, Mice, Inbred C57BL, Neuronal Plasticity, Restraint, Physical, Stress, Psychological, Signal Transduction, CREB-Binding Protein, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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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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