scholarly journals Preischemic Treadmill Exercise Ameliorates Memory Impairment and Microvasculature Damage in Rat Model of Chronic Cerebral Hypoperfusion

2021 ◽  
Vol 25 (Suppl 2) ◽  
pp. S72-80
Author(s):  
Jae-Min Lee ◽  
Jongmin Park ◽  
Joo-Hee Lee ◽  
Min Kyung Song ◽  
Youn-Jung Kim
Keyword(s):  
Cerebral Ischemia ◽  
Spatial Learning ◽  
Memory Impairment ◽  
Treadmill Exercise ◽  
Chronic Cerebral Hypoperfusion ◽  
Treadmill Running ◽  
Cerebral Hypoperfusion ◽  
Morris Water Maze Test ◽  
Sirt1 Expression ◽  
Spatial Learning Memory

Purpose: Silent information regulator 1 (SIRT1) in the brain is essential for maintaining cellular homeostasis and plays a neuroprotective role in cerebral ischemia and neurodegenerative disorders. The effect of preischemic treadmill exercise on chronic cerebral hypoperfusion (CCH)-induced spatial learning memory impairment, microvascular injury, and blood-brain barrier (BBB) disruption in relation with SIRT1 expression was evaluated.Methods: Prior to bilateral common carotid artery occlusion (BCCAO) surgery, the rats in the exercise groups performed low-intensity treadmill running for 30 minutes once daily during 8 weeks. BCCAO surgery was performed on male Wistar rats at 12 weeks of age. Spatial learning memory was measured using the Morris water maze test. Neuronal nuclear antigen, SIRT1, and rat endothelial cells antigen 1 were determined by immunohistochemistry and platelet-derived growth factor receptor beta was determined by immunofluorescence.Results: Preischemic treadmill exercise ameliorated spatial learning memory impairment and enhanced SIRT1 expression in the BCCAO rats. Preischemic treadmill exercise ameliorated BCCAO-induced damage to microvasculature and pericytes that make up the BBB. The effect of preischemic treadmill exercise was lost with sirtinol treatment.Conclusions: These results can apply treadmill exercise prior to cerebral ischemia as a rational preventive and therapeutic intervention strategy to improve cognitive dysfunction in CCH patients.

scholarly journals GABAB receptor antagonist promotes hippocampal neurogenesis and facilitates cognitive function recovery following acute cerebral ischemia in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Dan Song ◽  
Yaohua Chen ◽  
Cheng Chen ◽  
Lili Chen ◽  
Oumei Cheng
Keyword(s):  
Cognitive Function ◽  
Cerebral Ischemia ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Hippocampal Neurogenesis ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
In Vitro Experiments ◽  
Adult Mice

Abstract Purpose and background Previous studies have suggested that promoting endogenous neurogenesis has great significance for the recovery of cognitive dysfunction caused by cerebral ischemia (CI). Pharmacological inhibition of GABAB receptor can enhance neurogenesis in adult healthy and depressed mice. In the study, we intended to investigate the effects of GABAB receptor antagonists on cognitive function and hippocampal neurogenesis in mice following CI. Methods Adult mice were subjected to bilateral common carotid artery occlusion (BCCAO) for 20 min to induce CI and treated with CGP52432 (antagonist of GABAB receptor, CGP, 10 mg/kg intraperitoneal injection) starting 24 h after CI. The Morris water maze test was performed to test spatial learning and memory at day 28. Immunofluorescence was applied to detect neurogenesis in the DG region at day 14 and 28. In in vitro experiments, cell proliferation was detected by CCK8 and immunofluorescence, and the expression of cAMP/CREB signaling pathway-related proteins was detected by ELISA assay and Western blot. Results CGP significantly improved spatial learning and memory disorders caused by CI, and it enhanced the proliferation of neural stem cells (NSCs), the number of immature neurons, and the differentiation from newborn cells to neurons. In vitro experiments further confirmed that CGP dose-dependently enhanced the cell viability of NSCs, and immunofluorescence staining showed that CGP promoted the proliferation of NSCs. In addition, treatment with CGP increased the expression of cAMP, PKA, and pCREB in cultured NSCs. Conclusion Inhibition of GABAB receptor can effectively promote hippocampal neurogenesis and improve spatial learning and memory in adult mice following CI.

Resveratrol ameliorates spatial learning memory impairment induced by Aβ 1–42 in rats

Neuroscience ◽  
2017 ◽  
Vol 344 ◽  
pp. 39-47 ◽  
Author(s):  
Rui Wang ◽  
Yu Zhang ◽  
Jianguo Li ◽  
Ce Zhang
Keyword(s):  
Spatial Learning ◽  
Memory Impairment ◽  
Spatial Learning Memory

scholarly journals Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zhao-Hui Yao ◽  
Xiao-li Yao ◽  
Shao-feng Zhang ◽  
Ji-chang Hu ◽  
Yong Zhang
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Synaptic Proteins ◽  
Cerebral Hypoperfusion ◽  
Spatial Learning And Memory ◽  
Pathophysiological Mechanism

Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.

scholarly journals Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

Stroke ◽  
2011 ◽  
Vol 42 (9) ◽  
pp. 2595-2604 ◽  
Author(s):  
Bo-Ryoung Choi ◽  
Sang Rim Lee ◽  
Jung-Soo Han ◽  
Sang-Keun Woo ◽  
Kyeong Min Kim ◽  
...  
Keyword(s):  
Rat Model ◽  
Memory Impairment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

Effects and Comparison of Curcumin on Morphology Changes of Chronic Cerebral Hypoperfusion in Young and Aged Rats

2015 ◽  
Vol 1120-1121 ◽  
pp. 842-846
Author(s):  
Dan Li ◽  
Yue Xiang ◽  
Xiong Zhang ◽  
Yu Li
Keyword(s):  
Cerebral Ischemia ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Age Difference ◽  
Dependent Manner ◽  
Aged Rats ◽  
Pathological Changes ◽  
Chronic Cerebral Ischemia ◽  
Ca1 Region

To observe the effect of curcumin on the morphology of the hippocampus in young and aged rats with vascular dementia (VD) induced by chronic cerebral hypoperfusion, then further investigate whether the effect of curcumin have any differences in age. Both young and aged Male Sprague-Dawley rats were randomly divided into normal control group, sham-operated group, 2VO group, 2VO+curcumin 50mg/Kg group and 2VO+curcumin 100mg/Kg goup. Permanent occlusion of bilateral common carotid arteries ligation (2VO) method was used to establish chronic cerebral ischemia model. The rats were injected intraperitoneally with curcumin or DMSO once daily for 30d. The pathological changes of CA1 region of the hippocampus were measured by HE staining and Nissl staining. Chronic cerebral ischemia led to pathological changes of young and aged rats, but no significant differences were found between the two ages of rats (t=0.658，P=0.523). Furthermore, curcumin could reduce the pathological injury of CA1 region of the hippocampus in young and aged VD rats, no significant differences were found between the two ages of rats (P=0.384，P=0.380). Curcumin can reduce the brain damage in young and aged VD rats in dose-dependent manner but without age difference. Our study suggests that the pathological injury of the hippocampus might be one of the mechanisms of curcumin’s protection effect of VD rats.

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