Effect of aerobic exercise on BDNF/proBDNF expression in the ischemic hippocampus and depression recovery of rats after stroke

Luo, Lu; Li, Congqin; Du, Xinxin; Shi, Qilin; Huang, Qiao; Xu, Xiangyu; Wang, Qiang

doi:10.1016/j.bbr.2018.11.037

Cited by 75 publications

(31 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Likewise, in this study, we found that the BDNF level in the MCAO group was lower than that in the control group. This is also consistent with some other animal experiments [ 45 , 46 ]. Meanwhile, at the downstream of the BDNF/TrkB signaling pathway, the changes in the TrkB level reflected those of BDNF in both our study and others [ 47 , 48 ].…”

Section: Discussionsupporting

confidence: 93%

Electroacupuncture on Trigeminal Nerve-Innervated Acupoints Ameliorates Poststroke Cognitive Impairment in Rats with Middle Cerebral Artery Occlusion: Involvement of Neuroprotection and Synaptic Plasticity

et al. 2020

View full text Add to dashboard Cite

Poststroke cognitive impairment (PSCI) is a severe sequela of stroke. There are no effective therapeutic options for it. In this study, we evaluated whether electroacupuncture (EA) on the trigeminal nerve-innervated acupoints could alleviate PSCI and identified the mechanisms in an animal model. The male Sprague-Dawley rat middle cerebral artery occlusion (MCAO) model was used in our study. EA was conducted on the two scalp acupoints, EX-HN3 (Yintang) and GV20 (Baihui), innervated by the trigeminal nerve, for 14 sessions, daily. Morris water maze and novel object recognition were used to evaluate the animal’s cognitive performance. Neuroprotection and synaptic plasticity biomarkers were analyzed in brain tissues. Ischemia-reperfusion (I/R) injury significantly impaired spatial and cognition memory, while EA obviously reversed cognitive deterioration to the control level in the two cognitive paradigms. Moreover, EA reversed the I/R injury-induced decrease of brain-derived neurotrophic factor, tyrosine kinase B, N-methyl-D-aspartic acid receptor 1, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor, γ-aminobutyric acid type A receptors, Ca2+/calmodulin-dependent protein kinase II, neuronal nuclei, and postsynaptic density protein 95 expression in the prefrontal cortex and hippocampus. These results suggest that EA on the trigeminal nerve-innervated acupoints is an effective therapy for PSCI, in association with mediating neuroprotection and synaptic plasticity in related brain regions in the MCAO rat model.

show abstract

Section: Discussionsupporting

confidence: 93%

Electroacupuncture on Trigeminal Nerve-Innervated Acupoints Ameliorates Poststroke Cognitive Impairment in Rats with Middle Cerebral Artery Occlusion: Involvement of Neuroprotection and Synaptic Plasticity

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown that lower BDNF levels in the brain are closely related to anxiety-like behaviors (Yu et al, 2012). Furthermore, decreased BDNF and TrkB levels induced by acute and chronic stress could result in dysregulation of neural development and neural plasticity, which are involved in the pathogenesis of affective disorders, such as depression (Luo et al, 2019). In the present study, PTSD reduced protein and mRNA expression levels of BDNF both in the HIP and PFC, which is consistent with similar findings in previous studies.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Effect of Post-traumatic Stress in Adolescence on Dendrite Development and H3K9me2/BDNF Expression in Male Rat Hippocampus and Prefrontal Cortex

Zhao

Wang

Jiang

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Exposure to a harsh environment in early life increases in the risk of post-traumatic stress disorder (PTSD) of an individual. Brain derived neurotrophic factor (BDNF) plays an important role in neurodevelopment in developmental stages. Both chronic and traumatic stresses induce a decrease in the level of BDNF and reduce neural plasticity, which is linked to the pathogenesis of PTSD. Also, studies have shown that stress alters the epigenetic marker H3K9me2, which can bind to the promoter region of the Bdnf gene and reduce BDNF protein level. However, the long-term effects of traumatic stress during adolescence on H3K9me2, BDNF expression and dendrite development are not well-known. The present study established a model of PTSD in adolescent rats using an inescapable foot shock (IFS) procedure. Anxiety-like behaviors, social interaction behavior and memory function were assessed by the open field test, elevated plus maze test, three-chamber sociability test and Morris water maze test. In addition, neuronal development and H3K9me2/BDNF expression in hippocampus (HIP) and prefrontal cortex (PFC) were evaluated by Golgi staining, western blotting, qRT-PCR analysis and CHIP-qPCR analysis. Additionally, the Unc0642, a small molecule inhibitor of histone methyltransferase (EHMT2) was used for intervention. The results showed that the IFS procedure induced the PTSD-like behaviors in rats, resulted in fewer dendrite branches and shorter dendrite length in CA1 of HIP and PFC, increased H3K9me2 level and decreased BDNF expression in HIP and PFC. Also, although all the changes can persist to adulthood, Unc0642 administration relieved most of alterations. Our study suggests that traumatic stress in adolescence leads to immediate and long-term mental disorders, neuronal morphological changes, lower BDNF level and increased H3K9me2 level in the HIP and PFC, indicating that H3K9me2/BDNF dysfunction plays a key role in pathogenesis of PTSD.

show abstract

“…In healthy humans, moderate to intense exercise is well known to enhance BDNF activity (Coelho et al, 2013;Griffin et al, 2011;Knaepen, Goekint, Heyman, & Meeusen, 2010;Szuhany, Bugatti, & Otto, 2015;Zoladz et al, 2008), particularly in males (Szuhany et al, 2015;Zoladz et al, 2008). In animal stroke models, aerobic exercise could increase the expression of BDNF and the ratio of mBDNF to proBDNF in the hippocampus, resulting in enhanced neurogenesis (Lan et al, 2014;Luo, Li, Du, et al, 2019). One recent study revealed that high-intensity interval training is superior to moderate intensity continuous training in regards to improving depression-like behaviors, neural plasticity, and increasing mBDNF/proBDNF ratio in the hippocampus, especially in the CA3 and DG regions in PSD rats (Luo, Li, Deng, et al, 2019).…”

Section: Targ E Ting B Dnf For Ps Dmentioning

confidence: 99%

Brain‐derived neurotrophic factor and post‐stroke depression

Zhang

Liao

2019

J of Neuroscience Research

View full text Add to dashboard Cite

Brain‐derived neurotrophic factor (BDNF) is well known to play a critical role in cognition. Its role in mood disorders, including post stroke depression (PSD), is also recognized with more evidence surfacing. In patients with PSD, their serum BNDF level is lower than in those without depression. Furthermore, antidepressants could enhance BDNF expression in the brain, resulting in an alleviation of depression symptoms. Such therapeutic effect can be abolished in animals with the BDNF gene deleted. In PSD patients, the presence of stroke may contribute to the development of depression, including affecting the expression of BDNF. However, the mechanisms of BDNF in the development of PSD remain largely unknown. Lower BDNF levels may have existed in some patients before stroke onset, making them vulnerable to develop depressive symptoms. Meanwhile, the hypoxic environment induced by stroke could possibly downregulate BDNF expression in the brain. Current antidepressant treatments are not specific for PSD and there is a lack of treatments to address the linkage between stroke and PSD. This review summarizes the current knowledge of BDNF in PSD. By regulating BDNF expression, a synergistic effect may be achieved when such treatments are applied together with existing antidepressants.

show abstract

Effect of aerobic exercise on BDNF/proBDNF expression in the ischemic hippocampus and depression recovery of rats after stroke

Cited by 75 publications

References 26 publications

Electroacupuncture on Trigeminal Nerve-Innervated Acupoints Ameliorates Poststroke Cognitive Impairment in Rats with Middle Cerebral Artery Occlusion: Involvement of Neuroprotection and Synaptic Plasticity

Electroacupuncture on Trigeminal Nerve-Innervated Acupoints Ameliorates Poststroke Cognitive Impairment in Rats with Middle Cerebral Artery Occlusion: Involvement of Neuroprotection and Synaptic Plasticity

Long-Term Effect of Post-traumatic Stress in Adolescence on Dendrite Development and H3K9me2/BDNF Expression in Male Rat Hippocampus and Prefrontal Cortex

Brain‐derived neurotrophic factor and post‐stroke depression

Contact Info

Product

Resources

About