Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model.

Inflammation and glutamate (GLU) are widely thought to participate in the pathogenesis of depression, and current evidence suggests that the development of depression is associated with the activation of the kynurenine pathway (KP). However, the exact mechanism of KP among the inflammation, GLU and depression remain poorly understood. In this study, we examined the involvement of KP, inflammation and GLU in depressive phenotype induced by chronic unpredictable mild stress (CUMS) in C57B/6 J mice.

Integrated meta-analysis, data mining, and animal experiments to investigate the efficacy and potential pharmacological mechanism of a TCM tonic prescription, Jianpi Tongmai formula, in depression.

Background: Depression is a common psychiatric disorder and has become a growing public health issue. Traditional Chinese medicine (TCM) tonic prescriptions have been clinically proven to be an effective treatment for depression.

Purpose: This study aimed to identify the core prescription to improve depression among the numerous TCM tonic prescriptions.

Astrocytic Kir4.1 regulates NMDAR/calpain signaling axis in lipopolysaccharide-induced depression-like behaviors in mice.

The activation of Nod-like receptor protein 3 (NLRP3) inflammasome propagates pro-inflammatory signaling cascades linking to depression-like behaviors. However, the signaling pathway contributing to NLRP3 inflammasome activation and depression-like behaviors is still not clear. In this study, we evidenced that lipopolysaccharide (LPS) injection (i.

Polygonatum sibiricum polysaccharide prevents depression-like behaviors by reducing oxidative stress, inflammation, and cellular and synaptic damage.

Ethnopharmacological Relevance: According to traditional Chinese medicine (TCM) theory (Yi Xue Zheng Zhuan), the main factors associated with the pathogenesis of depression are deficiencies relating to five zang organs, Qi, and blood. Polygonatum sibiricum F. Delaroche (PS), which may avert these pathological changes, has been used in a variety of formulas to treat depression.

Ginsenoside Rg1 Prevents PTSD-Like Behaviors in Mice Through Promoting Synaptic Proteins, Reducing Kir4.1 and TNF-α in the Hippocampus.

Ginsenoside Rg1 is efficient to prevent or treat mental disorders. However, the mechanisms underlying the effects of ginsenoside Rg1 on post-traumatic stress disorder (PTSD) are still not known. In this study, single-prolonged stress (SPS) regime, as well as injection of lipopolysaccharide (LPS), was used to produce PTSD-like behaviors in C57 mice, and the effects of ginsenoside Rg1 (10, 20, 40 mg/kg/d, ip, for 14 days) on PTSD-like behaviors were evaluated.

Curculigoside facilitates fear extinction and prevents depression-like behaviors in a mouse learned helplessness model through increasing hippocampal BDNF.

Curculigoside (CUR) is the main active component of traditional Chinese medicine Curculigoorchioides Gaertn (Xianmao in Chinese), which exhibits a variety of pharmacological activities. In this study we investigated the effects of CUR on fear extinction and related depression-like behaviors in mice. In fear conditioning task, we found that administration of CUR (1.

Postnatal calpeptin treatment causes hippocampal neurodevelopmental defects in neonatal rats.

Our previous studies showed that the early use of calpain inhibitors reduces calpain activity in multiple brain regions, and that postnatal treatment with calpeptin may lead to cerebellar motor dysfunction. However, it remains unclear whether postnatal calpeptin application affects hippocampus-related behaviors. In this study, Sprague-Dawley rats were purchased from the Animal Center of Anhui Medical University of China.

Basolateral amygdala calpain is required for extinction of contextual fear-memory.

Extinction of fear-memory is essential for emotional and mental changes. However, the mechanisms underlying extinction of fear-memory are largely unknown. Calpain is a type of calcium-dependent protease that plays a critical role in memory consolidation and reconsolidation.