The Impacts of Swimming Exercise on Hippocampal Expression of Neurotrophic Factors in Rats Exposed to Chronic Unpredictable Mild Stress

Jiang, Pei; Dang, Ruili; Huan-de, LI; Zhang, Lihong; Zhu, Wenye; Xue, Ying; Tang, Mimi

doi:10.1155/2014/729827

Cited by 59 publications

(53 citation statements)

References 37 publications

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“…Increased GDNF mRNA expression in the hippocampus was also reported in a chronic unpredictable mild stress-induced depression model of rats [32]. However, a recent clinical investigation reported that the blood concentration of GDNF decreased in depressed patients [23], while antidepressant fluoxetine treatment in an animal model of Parkinson’s disease induced GDNF mRNA expression [33].…”

Section: Discussionmentioning

confidence: 99%

Astrocyte-Conditioned Medium Protects Prefrontal Cortical Neurons from Glutamate-Induced Cell Death by Inhibiting TNF-α Expression

Song

Yang

et al. 2019

Neuroimmunomodulation

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Objective: Both excitotoxicity and neurotrophin deficiency may contribute to the etiology of depression and neurodegeneration. Astrocytes not only regulate glutamate metabolism and clearance, they also produce neurotrophins in the brain. However, the direct interaction between neurons and astrocytes remains unknown. Methods: This study evaluated the cellular mechanisms by which astrocyte-conditioned medium (ACM) protects prefrontal cortical neurons from glutamate-induced death by measuring cell viability and morphology as well as mRNA and protein expression of brain-derived neurotrophic factor (BDNF), BDNF receptors, glial cell line-derived neurotrophic factor (GDNF), and the proinflammatory cytokine, tumor necrosis factor (TNF)-α. Neurons and astrocytes were purified from the brains of neonatal 1-day-old Sprague-Dawley rats. ACM was harvested after exposing astrocytes to culture medium containing 100 μM glutamate for 48 h. Results: Glutamate insult (100 μM for 6 h) significantly reduced neuronal cell viability and increased the mRNA expression of BDNF. Glutamate (24 h) decreased neuronal viability and the expression of BDNF, but increased mRNA expression of GFAP, p75 neurotrophin receptor (p75^NTR), and TNF-α. ACM pretreatment (2 h) reversed glutamate-decreased cell viability and increased BDNF, but reduced the expression of GDNF, P75^NTR, and TNF-α at the mRNA level. Western blotting generally confirmed the mRNA expression following 24 glutamate insults. Furthermore, the glutamate-induced decrease in the protein expression of BDNF and full-length TrkB receptor and increase in pro-BDNF, truncated TrkB isoform 1 receptor, p75^NTR, GDNF, and TNF-α were significantly attenuated by ACM pretreatment. Conclusions: The study demonstrates that ACM exerts neuroprotective effects on cell viability, and this effect is most likely mediated through the modulation of neurotrophin and TNF-α expression.

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Section: Discussionmentioning

confidence: 99%

Astrocyte-Conditioned Medium Protects Prefrontal Cortical Neurons from Glutamate-Induced Cell Death by Inhibiting TNF-α Expression

Song

Yang

et al. 2019

Neuroimmunomodulation

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“…For example, enhanced level of caspase-3 (encoded by the CASP3 gene) -a proteolytic enzyme inducing cellular apoptosis -was observed in the cerebral cortex of rats, which experienced chronic mild stress (Bachis et al, 2008). Moreover, a prolonged exposure to stress results in a reduced expression of the antiapoptotic BCL-XL gene and enhanced expression of the proapoptotic BAX gene; whereas, reduced stress exposure promoted expression of the brain-derived neurotrophic factor (BDNF), nerve growth factor (VGF) and neuropeptide (NPY) genes in the hippocampus (Jiang et al, 2014).…”

Section: Molecular Genetic Studies Of Depressive Disordersmentioning

confidence: 99%

Genetic basis of depressive disorders

Давыдова¹,

Enikeeva²,

Казанцева³

et al. 2019

Vestn. VOGiS

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Depression is a common mental disorder being one of the main causes of disability and mortality worldwide. Despite an intensive research during the past decades, the etiology of depressive disorders (DDs) remains incompletely understood; however, genetic factors are significantly involved in the liability to depression. The present review is focused on the studies based on a candidate gene approach, genome-wide association studies (GWAS) and whole exome sequencing (WES), which previously demonstrated associations between gene polymorphisms and DDs. According to the first approach, DD development is affected by serotonergic (TPH1, TPH2, HTR1A, HTR2A, and SLC6A4), dopaminergic (DRD4, SLC6A3) and noradrenergic (SLC6A2) system genes, and genes of enzymatic degradation (MAOA, COMT). In addition, there is evidence of the involvement of HPA-axis genes (OXTR, AVPR1A, and AVPR1B), sex hormone receptors genes (ESR1, ESR2, and AR), neurotrophin (BDNF) and methylenetetrahydrofolate reductase (MTHFR) genes, neuronal apoptosis (CASP3, BCL-XL, BAX, NPY, APP, and GRIN1) and inflammatory system (TNF, CRP, IL6, IL1B, PSMB4, PSMD9, and STAT3) genes in DD development. The results of the second approach (GWAS and WES) revealed that the PCLO, SIRT1, GNL3, GLT8D1, ITIH3, MTNR1A, BMP5, FHIT, KSR2, PCDH9, and AUTS2 genes predominantly responsible for neurogenesis and cell adhesion are involved in liability to depression. Therefore, the findings discussed suggest that genetic liability to DD is a complex process, which assumes simultaneous functioning of multiple genes including those reported previously, and requires future research in this field.

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“…Different signaling pathways were reported to be involved in the upregulation of hippocampal neurogenesis, such as growth factor signaling (e.g. BDNF, VEGF) [63][64][65], short peptides (e.g. leptin, adiponectin) [66,67], and cell cycle regulation (e.g.…”

Section: Exercise and Adult Neurogenesis: Serotonin Signalingmentioning

confidence: 99%

Neural Mechanisms of Exercise: Anti-Depression, Neurogenesis, and Serotonin Signaling

Yuan¹,

Paes²,

Arias-Carrión³

et al. 2015

CNSNDDT

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Depression is associated with decreased serotonin metabolism and functioning in the central nervous system, evidenced by both animal models of depression and clinical patient studies. Depression is also accompanied by decreased hippocampal neurogenesis in diverse animal models. Neurogenesis is mainly defined in dentate gyrus of hippocampus as well as subventricular zone. Moreover, hypothalamus, amygdala, olfactory tubercle, and piriform cortex are reported with evidences of adult neurogenesis. Physical exercise is found to modulate adult neurogenesis significantly, and results in mood improvement. The cellular mechanism such as adult neurogenesis upregulation was considered as one major mood regulator following exercise. The recent advances in molecular mechanisms underlying exercise-regulated neurogenesis have widen our understanding in brain plasticity in physiological and pathological conditions, and therefore better management of different psychiatric disorders.

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The Impacts of Swimming Exercise on Hippocampal Expression of Neurotrophic Factors in Rats Exposed to Chronic Unpredictable Mild Stress

Cited by 59 publications

References 37 publications

Astrocyte-Conditioned Medium Protects Prefrontal Cortical Neurons from Glutamate-Induced Cell Death by Inhibiting TNF-α Expression

Astrocyte-Conditioned Medium Protects Prefrontal Cortical Neurons from Glutamate-Induced Cell Death by Inhibiting TNF-α Expression

Genetic basis of depressive disorders

Neural Mechanisms of Exercise: Anti-Depression, Neurogenesis, and Serotonin Signaling

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