ArticleActa neuropathologica2021
PSD-93 up-regulates the synaptic activity of corticotropin-releasing hormone neurons in the paraventricular nucleus in depression.
Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Epigenome-wide association studies of prenatal maternal mental health and infant epigenetic profiles: a systematic review.Translational psychiatry · 2023Pooled it
- Whole-Brain Monosynaptic Inputs and Outputs of Corticotropin-Releasing Hormone Neurons of the Paraventricular Nucleus of the Hypothalamus in Male Mice.CNS neuroscience & therapeutics · 2026Article
- Hypothalamic Oxytocin Neuronal Activation Induces Bipolar-Like Mood Changes in Mice in a Sex- and Dosage-Dependent Manner.Neuroscience bulletin · 2026Article
- Acute systemic inflammation induces region-specific morphological remodeling of astrocytes and microglia concurrent with depression-like behavior.Histochemistry and cell biology · 2025Article
- Overactivation of PERK-Mediated Endoplasmic Reticulum Stress-Induced Testis Damage in Chronically Stressed Mice.ACS omega · 2025Article
- Inhibition of Ephrin receptor signaling in the paraventricular nucleus attenuates psoriasis-like dermatitis via synaptic plasticity and immune homeostasis modulation.Journal of neuroinflammation · 2025Article
- Electroacupuncture ameliorates visceral hypersensitivity and negative emotions by regulating paraventricular hypothalamic nucleus and colonic corticotropin-releasing factor signaling.World journal of psychiatry · 2025Article
- The Hypothalamic Medial Preoptic Area-Paraventricular Nucleus Circuit Modulates Depressive-Like Behaviors in a Mouse Model of Postpartum Depression.Research (Washington, D.C.) · 2025Article
- Biological Basis for the Formation of Suicidal Behavior: A Review.Medical journal of the Islamic Republic of Iran · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- Polysaccharides fromHeliyon · 2024Article
- Research Progress of Central and Peripheral Corticotropin-Releasing Hormone in Irritable Bowel Syndrome with Comorbid Dysthymic Disorders.Gut and liver · 2024Review
- Increased cysteinyl-tRNA synthetase drives neuroinflammation in Alzheimer's disease.Translational neurodegeneration · 2024Article
- A tool kit of highly selective and sensitive genetically encoded neuropeptide sensors.Science (New York, N.Y.) · 2023Article
- The PrLiScience · 2023Article
- Recent advances in the study of sepsis-induced depression.Journal of intensive medicine · 2023Review
- Electroacupuncture alleviates perioperative hypothalamus-pituitary-adrenal axis dysfunctionFrontiers in molecular neuroscience · 2023Article
- Brain-Type Glycogen Phosphorylase Is Crucial for Astrocytic Glycogen Accumulation in Chronic Social Defeat Stress-Induced Depression in Mice.Frontiers in molecular neuroscience · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the discovery of ketamine anti-depressant effects in last decade, it has effectively revitalized interest in investigating excitatory synapses hypothesis in the pathogenesis of depression. In the present study, we aimed to reveal the excitatory synaptic regulation of corticotropin-releasing hormone (CRH) neuron in the hypothalamus, which is the driving force in hypothalamic-pituitary-adrenal (HPA) axis regulation. This study constitutes the first observation of an increased density of PSD-93-CRH co-localized neurons in the hypothalamic paraventricular nucleus (PVN) of patients with major depression. PSD-93 overexpression in CRH neurons in the PVN induced depression-like behaviors in mice, accompanied by increased serum corticosterone level. PSD-93 knockdown relieved the depression-like phenotypes in a lipopolysaccharide (LPS)-induced depression model. Electrophysiological data showed that PSD-93 overexpression increased CRH neurons synaptic activity, while PSD-93 knockdown decreased CRH neurons synaptic activity. Furthermore, we found that LPS induced increased the release of glutamate from microglia to CRH neurons resulted in depression-like behaviors using fiber photometry recordings. Together, these results show that PSD-93 is involved in the pathogenesis of depression via increasing the synaptic activity of CRH neurons in the PVN, leading to the hyperactivity of the HPA axis that underlies depression-like behaviors.
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