PSD-93 up-regulates the synaptic activity of corticotropin-releasing hormone neurons in the paraventricular nucleus in depression

Qin, Xin-Ya; Shan, Qing-Hong; Fang, Hui; Wang, Yu; Chen, Peng; Xiong, Zhi‐Qi; Swaab, D.F.; Zhou, Jiang‐Ning

doi:10.1007/s00401-021-02371-7

Cited by 21 publications

(12 citation statements)

References 95 publications

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“…The results of FISH showed an increase in the fluorescence intensity of glutaminase co‐localized with Iba1 + ‐microglia in the PVN after 6 h of LPS treatment. Further glutamate sensor detection (iGluSnFR) and fiber photometry recordings demonstrated that the increase in total glutamate events is mediated by tight membrane‐membrane contacts and functional connections between activated microglia and the neighboring PSD‐93‐immunoreactive neurons after LPS treatment (Qin et al, 2021).…”

Section: Microglia and Synaptic Transmissionmentioning

confidence: 99%

“…Taken together, microglia regulate synaptic transmission by secreting NTFs, cytokines, MVs, and transmitters and by controlling the morphological changes of synapses through synaptic pruning and phagocytosis under physiological and pathological conditions (Prinz et al, 2019; Qin et al, 2021; Tapanes et al, 2022). Recently, Akiyoshi et al used two‐photon imaging in vivo to demonstrate that the brief contacts between microglial processes and synapses in the primary motor cortex of healthy mice result in more Ca 2+ transients in dendritic spines, reflecting enhanced synaptic activity (Akiyoshi et al, 2018).…”

Section: Microglia and Synaptic Transmissionmentioning

confidence: 99%

“…reported that the expression of glutaminase in microglia and the release of glutamate to corticotrophin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus (PVN) are increased in an LPS-induced depression mouse model. The results of FISH showed an increase in the fluorescence intensity of glutaminase colocalized with Iba1 + -microglia in the PVN after 6 h of LPS treatment.Further glutamate sensor detection (iGluSnFR) and fiber photometry recordings demonstrated that the increase in total glutamate events is mediated by tight membrane-membrane contacts and functional connections between activated microglia and the neighboring PSD-93-immunoreactive neurons after LPS treatment(Qin et al, 2021).Additionally, Tapanes et al reported that TBI-induced synaptic damage and memory impairment require D-serine synthesis and release from reactive microglia. Using fluorescence-activated cell sorting (FACS) and high-performance liquid chromatography (HPLC) analysis, Tapanes et al demonstrated that SR and D-serine levels were increased in hippocampal microglia after controlled cortical impact (CCI) injury, which contributed to NMDAR-mediated synaptic damage and memory impairment via the transporter Slc1a4 (ASCT1), representing the first study to identify a pathological role for microglialderived D-serine in vivo following brain trauma(Tapanes et al, 2022).…”

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confidence: 99%

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Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells

Liu

Shen

Zhang

et al. 2023

Glia

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The mammalian brain is a complex organ comprising neurons, glia, and more than 1 × 1014 synapses. Neurons are a heterogeneous group of electrically active cells, which form the framework of the complex circuitry of the brain. However, glial cells, which are primarily divided into astrocytes, microglia, oligodendrocytes (OLs), and oligodendrocyte precursor cells (OPCs), constitute approximately half of all neural cells in the mammalian central nervous system (CNS) and mainly provide nutrition and tropic support to neurons in the brain. In the last two decades, the concept of “tripartite synapses” has drawn great attention, which emphasizes that astrocytes are an integral part of the synapse and regulate neuronal activity in a feedback manner after receiving neuronal signals. Since then, synaptic modulation by glial cells has been extensively studied and substantially revised. In this review, we summarize the latest significant findings on how glial cells, in particular, microglia and OL lineage cells, impact and remodel the structure and function of synapses in the brain. Our review highlights the cellular and molecular aspects of neuron‐glia crosstalk and provides additional information on how aberrant synaptic communication between neurons and glia may contribute to neural pathologies.

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Section: Microglia and Synaptic Transmissionmentioning

confidence: 99%

Section: Microglia and Synaptic Transmissionmentioning

confidence: 99%

mentioning

confidence: 99%

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Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells

Liu

Shen

Zhang

et al. 2023

Glia

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“…The hypothalamic–pituitary–adrenal (HPA) axis plays an important role in stress responses ( Heck and Handa, 2019 ; Frankiensztajn et al, 2020 ), and HPA hyperactivity is associated with surgery-induced acute stress in clinical practice ( Spencer-Segal et al, 2020 ; Zhu et al, 2021 ). Previous studies have shown that surgical trauma aggravates hyperactivity of the HPA axis, which is characterized by excessive release of hypothalamic corticotrophin-releasing hormone (CRH), peripheral adrenocorticotropic hormone (ACTH), and corticosterone (CORT; Qin et al, 2021 ). The pathophysiological events associated with the HPA axis can also trigger secondary effects such as abnormal metabolism ( Mi et al, 2019 ), immunosuppression ( Kim et al, 2019 ), neuroinflammation ( Cernackova et al, 2020 ), hypertension ( Hepsen et al, 2020 ), and multiple system dysfunction ( Keller et al, 2017 ; Juruena et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture alleviates perioperative hypothalamus-pituitary-adrenal axis dysfunction via circRNA-miRNA-mRNA networks

Wang

Zheng

et al. 2023

Front. Mol. Neurosci.

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Electroacupuncture (EA) has long been used to alleviate surgery-induced hypothalamic–pituitary–adrenal axis dysfunction. However, its downstream gene targets in the brain remain unclear. The aim of the present study was to clarify the potential targets of EA based on RNA sequencing techniques (RNA-seq). Rats were divided into normal control (NC), hepatectomy surgery (HT), HT + EA, and HT + sham EA groups followed by RNA-seq of two representative nuclei in the hypothalamus and amygdala. Weighted Gene Co-expression Network Analysis and Gene Set Enrichment Analysis identified six gene modules associated with neuroendocrine transmitters and neural remodeling in the hypothalamus. Furthermore, circRNA-miRNA-mRNA interaction networks revealed EA-related candidate miRNAs and circRNAs, of which opioid receptor mu 1 might be an EA-specific target, and showed regulation by competing endogenous RNA. We identified the neuroendocrine circRNA-miRNA-mRNA networks through which EA has an effect on HPA axis dysfunction, thus providing potential targets and future research directions for EA treatment.

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“…Mostly, a disturbed monoamine transmission is considered to be involved in the pathogenesis of depression. However, growing evidence suggests that the hypothalamic-pituitary-adrenal axis and proinflammatory cytokines also play important roles ( Hayley et al, 2021 ; Qin et al, 2021 ). The fact that current treatment strategies are not useful in some patients evidences our incomplete understanding of the disease etiology.…”

Section: Introductionmentioning

confidence: 99%

Brain-Type Glycogen Phosphorylase Is Crucial for Astrocytic Glycogen Accumulation in Chronic Social Defeat Stress-Induced Depression in Mice

Zhu

Fan

Zhao

et al. 2022

Front. Mol. Neurosci.

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Astrocytic glycogen plays an important role in brain energy metabolism. However, the contribution of glycogen metabolism to stress-induced depression remains unclear. Chronic social defeat stress was used to induce depression-like behaviors in mice, assessed with behavioral tests. Glycogen concentration in the medial prefrontal cortex (mPFC) and the expression of key enzymes of the glycogen metabolism were investigated using Western blots, immunofluorescent staining, electron microscopy, and biochemical assays. Stereotaxic surgery and viral-mediated gene transfer were applied to knockdown or overexpress brain-type glycogen phosphorylase (PYGB) in the mPFC. The glycogen content increased in the mPFC after stress. Glycogenolytic dysfunction due to inactivation of PYGB was responsible for glycogen accumulation. Behavioral tests on astrocyte-specific PYGB overexpression mice showed that augmenting astrocytic PYGB reduces susceptibility to depression when compared with stress-susceptible mice. Conversely, PYGB genetic down-regulation in the mPFC was sufficient to induce glycogen accumulation and depression-like behaviors. Furthermore, PYGB overexpression in the mPFC decreases susceptibility to depression, at least partially by rescuing glycogen phosphorylase activity to maintain glycogen metabolism homeostasis during stress. These findings indicate that (1) glycogen accumulation occurs in mice following stress and (2) glycogenolysis reprogramming leads to glycogen accumulation in astrocytes and PYGB contributes to stress-induced depression-like behaviors. Pharmacological tools acting on glycogenolysis might constitute a promising therapy for depression.

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PSD-93 up-regulates the synaptic activity of corticotropin-releasing hormone neurons in the paraventricular nucleus in depression

Cited by 21 publications

References 95 publications

Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells

Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells

Electroacupuncture alleviates perioperative hypothalamus-pituitary-adrenal axis dysfunction via circRNA-miRNA-mRNA networks

Brain-Type Glycogen Phosphorylase Is Crucial for Astrocytic Glycogen Accumulation in Chronic Social Defeat Stress-Induced Depression in Mice

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