Hippocampal F3/Contactin plays a role in chronic stress-induced depressive-like effects and the antidepressant actions of vortioxetine in mice

Chen, Yanmei; Fan, Huahao; Huang, Jie; Shi, Tian-Shun; Li, Wei-Yu; Wang, Chengniu; Jiang, Bo; Liu, Jianfeng

doi:10.1016/j.bcp.2022.115097

Cited by 7 publications

(4 citation statements)

References 57 publications

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“…The SPT was per-formed using previously reported methods with modi cations [29] . Before testing, mice were supplied with one bottle of 1% sucrose water (w/v) and one bottle of puri ed water for 24 h. Then, the mice were fasted and deprived of water for 12 h. Pre-weighed sucrose and distilled water bottles were placed on the cages, and the mice drank water freely for 6 h. During this period, the position of the two water bottles was changed every 3 h. At the end of the experiment, the two water bottles were weighed.…”

Section: Sucrose Preference Test (Spt)mentioning

confidence: 99%

Ethanol extract of Alpiniae oxyphyllae fructus regulates glucose metabolism, the HPA axis and hippocampal function in diabetic mice with depression

Zhou,

Qi,

Deng

et al. 2023

Preprint

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Background: Alpiniae oxyphyllae fructus (AOF) is the dry ripe fruit of Alpinia oxyphylla Miq. which has significant therapeutic effects in Alzheimer's disease, Parkinson's disease, depression, learning and memory dysfunction and other nervous system disease. Methods: In this study, we established a mouse model of Type 2 Diabetes Mellitus (T2DM) combined with depression induced by feeding high fat and high sugar diet combined with intraperitoneal injection of streptozotocin (STZ) and chronic unpredictable mild stress (CUMS) to evaluate the dual therapeutic effects of ethanol extract of AOF (EEA), and further explore the mechanism of EEA on diabetes complicated with depression. Results: The results showed that EEA improved the body weight of diabetic mice with depression (DD mice). EEA could also improve glucose metabolism and insulin resistance in DD mice. Next, EEA improved the depression-like behaviors of DD mice. EEA also attenuated diabetes and CUMS-induced hyperactivity of the hypothalamic-pituitary-adrenal(HPA) axis and improved the expression of neurotransmitters and synaptic plasticity in the hippocampus of DD mice. In addition, EEA could improve hippocampal tissue damage caused by neuroinflammation and oxidative stress. Further research showed that EEA improved the protein expression and phosphorylation of Phosphoinositide 3-kinase (PI3K), Protein kinase B (Akt) and Mammalian target of rapamycin (mTOR) in the hippocampus of DD mice. Conclusions: This study showed that EEA may have a dual role in the treatment of diabetes and depression and provided new scientific theoretical basis for the future development of AOF and the prevention and treatment of diabetes complicated with depression.

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Section: Sucrose Preference Test (Spt)mentioning

confidence: 99%

Ethanol extract of Alpiniae oxyphyllae fructus regulates glucose metabolism, the HPA axis and hippocampal function in diabetic mice with depression

Zhou,

Qi,

Deng

et al. 2023

Preprint

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“…Estrogen deficiency can cause depression-like behavior, and Huang et al (44) found in their experiments that estrogen deficiency-induced depression was associated with intestinal flora imbalance and inflammatory response in mice undergoing ovariectomy (OVX), where intestinal flora imbalance caused (45). There is growing evidence that modulation of BDNF expression levels can exert antidepressant effects (46)(47)(48), where BDNF-cAMP response element binding protein (CREB) signaling is one of the most attractive signaling pathways for the treatment of depression (49,50). In summary, gut flora and COX-2mediated inflammatory responses are strongly correlated, but there are fewer studies on how COX-2-mediated pathways and gut flora-brain centers interact and thus mediate depression, and further research is needed (Figure 1).…”

Section: Intestinal Flora Dysbiosismentioning

confidence: 99%

“…BDNF is a neuroprotective molecule that plays a key role in neuroplasticity, neuroinflammation, learning and memory ( 45 ). There is growing evidence that modulation of BDNF expression levels can exert antidepressant effects ( 46 – 48 ), where BDNF-cAMP response element binding protein (CREB) signaling is one of the most attractive signaling pathways for the treatment of depression ( 49 , 50 ). In summary, gut flora and COX-2-mediated inflammatory responses are strongly correlated, but there are fewer studies on how COX-2-mediated pathways and gut flora-brain centers interact and thus mediate depression, and further research is needed ( Figure 1 ).…”

Section: Cyclo-oxygen-ase-2 Roles In the Pathogenesis Of Depressionmentioning

confidence: 99%

Biology of cyclooxygenase-2: An application in depression therapeutics

Han

Liao

et al. 2022

Front. Psychiatry

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Depressive Disorder is a common mood disorder or affective disorder that is dominated by depressed mood. It is characterized by a high incidence and recurrence. The onset of depression is related to genetic, biological and psychosocial factors. However, the pathogenesis is still unclear. In recent years, there has been an increasing amount of research on the inflammatory hypothesis of depression, in which cyclo-oxygen-ase 2 (COX-2), a pro-inflammatory cytokine, is closely associated with depression. A variety of chemical drugs and natural products have been found to exert therapeutic effects by modulating COX-2 levels. This paper summarizes the relationship between COX-2 and depression in terms of neuroinflammation, intestinal flora, neurotransmitters, HPA axis, mitochondrial dysfunction and hippocampal neuronal damage, which can provide a reference for further preventive control, clinical treatment and scientific research on depression.

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“…It is now thought that a requirement for intracellular signaling cascade adaptations could account for the time delay (weeks to months) in the therapeutic responses to clinical antidepressants such as serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors ( Berton and Nestler, 2006 ). According to this opinion, more novel targets for antidepressant therapies have been reported ( Chen et al, 2022 ; Jiang et al, 2019 ; Wang et al, 2020a ; Guan et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Activation of mTORC1 Signaling Cascade in Hippocampus and Medial Prefrontal Cortex Is Required for Antidepressant Actions of Vortioxetine in Mice

Shi

Huang

et al. 2023

International Journal of Neuropsychopharmacology

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Background Although thought as a multimodal-acting antidepressant targeting at the serotonin system, more and more other molecules are being reported to participate in the antidepressant mechanism of vortioxetine. A previous report has shown that vortioxetine administration enhanced the expression of rapamycin complex 1 (mTORC1) in neurons. It has been well demonstrated that mTORC1 participates in not only the pathogenesis of depression but also the pharmacological mechanisms of many antidepressants. Therefore, we speculate that the antidepressant mechanism of vortioxetine may require mTORC1. Methods Two mice models of depression (chronic social defeat stress and chronic unpredictable mild stress) and western blotting were first used together to examine whether vortioxetine administration produced reversal effects against the chronic stress-induced down-regulation in the whole mTORC1 signaling cascade in both the hippocampus and medial prefrontal cortex. Then, LY294002, U0126, and rapamycin were used together to explore whether the antidepressant effects of vortioxetine in mice models of depression were attenuated by pharmacological blockade of the mTORC1 system. Furthermore, LV-mTORC1-shRNA-EGFP was adopted to examine if genetic blockade of mTORC1 also abolished the antidepressant actions of vortioxetine in mice. Results Vortioxetine administration produced significant reversal effects against the chronic stress-induced down-regulation in the whole mTORC1 signaling cascade in both the hippocampus and medial prefrontal cortex. Both pharmacological and genetic blockade of the mTORC1 system notably attenuated the antidepressant effects of vortioxetine in mice. Conclusions Activation of the mTORC1 system in the hippocampus and medial prefrontal cortex is required for the antidepressant actions of vortioxetine in mice.

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Hippocampal F3/Contactin plays a role in chronic stress-induced depressive-like effects and the antidepressant actions of vortioxetine in mice

Cited by 7 publications

References 57 publications

Ethanol extract of Alpiniae oxyphyllae fructus regulates glucose metabolism, the HPA axis and hippocampal function in diabetic mice with depression

Ethanol extract of Alpiniae oxyphyllae fructus regulates glucose metabolism, the HPA axis and hippocampal function in diabetic mice with depression

Biology of cyclooxygenase-2: An application in depression therapeutics

Activation of mTORC1 Signaling Cascade in Hippocampus and Medial Prefrontal Cortex Is Required for Antidepressant Actions of Vortioxetine in Mice

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