Chronic intermittent hypoxia impairs synaptic plasticity and expression of brain-derived neurotrophic factor in mouse hippocampus

2010 ◽  
Vol 68 ◽  
pp. e174
Author(s):  
Hui Xie ◽  
Kin-Ling Leung ◽  
Albert M. Li ◽  
Wing-Ho Yung
2016 ◽  
Vol 131 (2) ◽  
pp. 123-138 ◽  
Author(s):  
Veronica Begni ◽  
Marco Andrea Riva ◽  
Annamaria Cattaneo

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that plays a key role in the central nervous system, promoting synaptic plasticity, neurogenesis and neuroprotection. The BDNF gene structure is very complex and consists of multiple 5′-non-coding exons, which give rise to differently spliced transcripts, and one coding exon at the 3′-end. These multiple transcripts, together with the complex transcriptional regulatory machinery, lead to a complex and fine regulation of BDNF expression that can be tissue and stimulus specific. BDNF effects are mainly mediated by the high-affinity, tropomyosin-related, kinase B receptor and involve the activation of several downstream cascades, including the mitogen-activated protein kinase, phospholipase C-γ and phosphoinositide-3-kinase pathways. BDNF exerts a wide range of effects on neuronal function, including the modulation of activity-dependent synaptic plasticity and neurogenesis. Importantly, alterations in BDNF expression and function are involved in different brain disorders and represent a major downstream mechanism for stress response, which has important implications in psychiatric diseases, such as major depressive disorders and schizophrenia. In the present review, we have summarized the main features of BDNF in relation to neuronal plasticity, stress response and pathological conditions, and discussed the role of BDNF as a possible target for pharmacological and non-pharmacological treatments in the context of psychiatric illnesses.


2020 ◽  
Vol 171 ◽  
pp. 107186
Author(s):  
Zhen Wang ◽  
Xiao Lin Zhong ◽  
Yang Xu ◽  
Jie He ◽  
Zheng Hai Liu ◽  
...  

2003 ◽  
Vol 23 (34) ◽  
pp. 10800-10808 ◽  
Author(s):  
Janet Alder ◽  
Smita Thakker-Varia ◽  
Debra A. Bangasser ◽  
May Kuroiwa ◽  
Mark R. Plummer ◽  
...  

2021 ◽  
Vol 19 (12) ◽  
pp. 2537-2543
Author(s):  
Xuping Wen ◽  
Mingshuan Lin

Purpose: To explore the effect of miR-195a on nerve cells in the hippocampal region of depressionmodel mice.Methods: A chronic social defeat stress (CSDS) model was used as a depressed mouse model. In vivo, C57BL/6J mice received CSDS treatment or miR-195a antagomir. Depression-like behaviors were evaluated. In vitro, the target relationship between miR-195a and brain-derived neurotrophic factor (BDNF) was validated by luciferase reporter assays in HEK-293 cells. In primary cortical neurons, expression levels of miR-195a and BDNF mRNA were evaluated using quantitative polymerase chain reaction (qPCR). BDNF protein expression was determined by western blotting.Results: The sucrose preference ratio and social contact of the CSDS group were significantly decreased, whereas the immobility time was significantly increased, compared with the control group (p< 0.05). Interestingly, the expression of miR-195a was upregulated in the CSDS group compared with control group (p < 0.05). Bioinformatics prediction and luciferase reporter assay data indicate that miR195a bound the BDNF 3’ untranslated region. BDNF protein expression levels were significantly reduced by miR-195a mimic but increased by miR-195a inhibitor, compared with the negative control mimic group (p < 0.05). In vivo, miR-195a antagomir alleviated depression-like behaviors compared with CSDS group. In addition, miR-195a antagomir restored the expression of BDNF in mouse hippocampus in the CSDS group (p < 0.05).Conclusion: MiR-195a inhibitor ameliorates depression-like behaviors of depressed mice by downregulation of BDNF, whereas  upregulation of miR-195a inhibits BDNF expression in mouse hippocampus and may contribute to depression. Keywords: Chronic social defeat stress, Depression, MiR-195, brain-derived neurotrophic factor, BDNF 


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