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327 results on '"Cui, Ranji"'

13. Rasd2 regulates depression-like behaviors via DRD2 neurons in the prelimbic cortex afferent to nucleus accumbens core circuit

Author

Cheng, Ziqian, Zhao, Fangyi, Piao, Jingjing, Yang, Wei, Cui, Ranji, and Li, Bingjin

Abstract

Depressive symptoms, such as anhedonia, decreased social interaction, and lack of motivation, implicate brain reward systems in the pathophysiology of depression. Exposure to chronic stress impairs the function of brain reward circuits and is well-known to be involved in the etiology of depression. A transcriptomic analysis found that stress alters the expression of Rasd2in mice prefrontal cortex (PFC). Similarly, in our previous study, acute fasting decreased Rasd2expression in mice PFC, and RASD2 modulated dopamine D2 receptor (DRD2)-mediated antidepressant-like effects in ovariectomized mice. This research suggests the role of RASD2 in stress-induced depression and its underlying neural mechanisms that require further investigation. Here, we show that 5-day unpredictable mild stress (5-d UMS) exposure reduces RASD2 expression in both the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) of mice, while overexpression (but not knock-down) of Rasd2in the NAc core (NAcc) alleviates 5-d UMS-induced depression-like behaviors and activates the DRD2-cAMP-PKA-DARPP-32 signaling pathway. Further studies investigated neuronal projections between the mPFC (Cg1, PrL, and IL) and NAcc, labeled by the retrograde tracer Fluorogold. Depression-like behaviors induced by 5-d UMS were only related to inhibition of the PrL-NAcc circuit. DREADD (Designer receptors exclusively activated by designer drug) analysis found that the activation of PrL-NAcc glutaminergic projection alleviated depression-like behaviors and increased DRD2- and RASD2-positive neurons in the NAcc. Using Drd2-cretransgenic mice, we constructed mice with Rasd2overexpression in DRD2PrL-NAccneurons, finding that Rasd2overexpression ameliorated 5-d UMS-induced depression-like behaviors. These findings demonstrate a critical role for RASD2 modulation of DRD2PrL-NAccneurons in 5-d UMS-induced depression-like behaviors. In addition, the study identifies a new potential strategy for precision medical treatment of depression.

Published
2024
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26. Berberine: A Promising Treatment for Neurodegenerative Diseases

Author

Cheng, Ziqian, primary, Kang, Chenglan, additional, Che, Songtian, additional, Su, Jingyun, additional, Sun, Qihan, additional, Ge, Tongtong, additional, Guo, Yi, additional, Lv, Jiayin, additional, Sun, Zhihui, additional, Yang, Wei, additional, Li, Bingjin, additional, Li, Xin, additional, and Cui, Ranji, additional

Published
2022
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40. Pharmacological effects of berberine on mood disorders

Author

Fan, Jie, Zhang, Kun, Jin, Yang, Li, Bingjini, Gao, Shuohui, Zhu, Jiaming, and Cui, Ranji

Subjects
0301 basic medicine, Hydrastis, Berberine, Central nervous system, Reviews, mechanism, Review, Pharmacology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Animals, Humans, Medicine, Bipolar disorder, Receptor, bipolar disorder, Depressive Disorder, Major, Mood Disorders, business.industry, Mechanism (biology), Alkaloid, Cell Biology, anxiety, medicine.disease, Antidepressive Agents, Neuroprotective Agents, 030104 developmental biology, medicine.anatomical_structure, chemistry, Mood disorders, 030220 oncology & carcinogenesis, depression, Molecular Medicine, Anxiety, Plant Preparations, pharmacology, medicine.symptom, business, Phytotherapy
Abstract

Berberine, a natural isoquinoline alkaloid, is used in herbal medicine and has recently been shown to have efficacy in the treatment of mood disorders. Furthermore, berberine modulates neurotransmitters and their receptor systems within the central nervous system. However, the detailed mechanisms of its action remain unclear. This review summarizes the pharmacological effects of berberine on mood disorders. Therefore, it may be helpful for potential application in the treatment of mood disorders.

Published
2018

43. Role of BDNF-mTORC1 Signaling Pathway in Female Depression

Author

An, Xianquan, Yao, Xiaoxiao, Li, Bingjin, Yang, Wei, Cui, Ranji, Zhao, Guoqing, and Jin, Yang

Subjects
Article Subject
Abstract

Depression is a common psychological and mental disorder, characterized by low mood, slow thinking and low will, and even suicidal tendencies in severe cases. It imposes a huge mental and economic burden on patients and their families, and its prevention and treatment have become an urgent public health problem. It is worth noting that there is a significant gender difference in the incidence of depression. Studies have shown that females are far more likely to suffer from depression than males, confirming a close relationship between estrogen and the onset of depression. Moreover, recent studies suggest that the brain-derived neurotrophic factor- (BDNF-) mammalian target of rapamycin complex-1 (mTORC1) signaling pathway is a crucial target pathway for improving depression and mediates the rapid antidepressant-like effects of various antidepressants. However, it is not clear whether the BDNF-mTORC1 signaling pathway mediates the regulation of female depression and how to regulate female depression. Hence, we focused on the modulation of estrogen-BDNF-mTORC1 signaling in depression and its possible mechanisms in recent years.

Published
2021
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46. Changes in Hippocampal Plasticity in Depression and Therapeutic Approaches Influencing These Changes

Author

Xu, Wenbo, Yao, Xiaoxiao, Zhao, Fangyi, Zhao, Haisheng, Cheng, Ziqian, Yang, Wei, Cui, Ranji, Xu, Songbai, and Li, Bingjin

Subjects
Article Subject, sense organs, skin and connective tissue diseases
Abstract

Depression is a common neurological disease that seriously affects human health. There are many hypotheses about the pathogenesis of depression, and the most widely recognized and applied is the monoamine hypothesis. However, no hypothesis can fully explain the pathogenesis of depression. At present, the brain-derived neurotrophic factor (BDNF) and neurogenesis hypotheses have highlighted the important role of plasticity in depression. The plasticity of neurons and glial cells plays a vital role in the transmission and integration of signals in the central nervous system. Plasticity is the adaptive change in the nervous system in response to changes in external signals. The hippocampus is an important anatomical area associated with depression. Studies have shown that some antidepressants can treat depression by changing the plasticity of the hippocampus. Furthermore, caloric restriction has also been shown to affect antidepressant and hippocampal plasticity changes. In this review, we summarize the latest research, focusing on changes in the plasticity of hippocampal neurons and glial cells in depression and the role of BDNF in the changes in hippocampal plasticity in depression, as well as caloric restriction and mitochondrial plasticity. This review may contribute to the development of antidepressant drugs and elucidating the mechanism of depression.

Published
2020
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47. Neuropharmacological Effects of Mesaconitine: Evidence from Molecular and Cellular Basis of Neural Circuit

Author

Sun, Zhihui, Yang, Limin, Zhao, Lihong, Cui, Ranji, and Yang, Wei

Subjects
Article Subject
Abstract

Mesaconitine (MA), a diester-diterpenoid alkaloid in aconite roots, is considered to be one of the most important bioactive ingredients. In this review, we summarized its neuropharmacological effects, including analgesic effects and antiepileptiform effects. Mesaconitine can act on the central noradrenergic system and the serotonin system; behaving like the norepinephrine reuptake inhibitors and tricyclic antidepressants that increase norepinephrine levels in stress-induced depression. Therefore, the possible perspectives for future studies on the depression of MA were also discussed as well. The pharmacological effect of MA on depression is worthy of further study.

Published
2020
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