scholarly journals Alternations of Septal-hippocampal System in the Adult Wistar Rat with Spatial Memory Impairments Induced by Chronic Cerebral Hypoperfusion

2011 ◽  
Vol 20 (2) ◽  
pp. 92-99 ◽  
Author(s):  
Bo-Ryoung Choi ◽  
Kyoung Ja Kwon ◽  
Seung Hwa Park ◽  
Won Kyung Jeon ◽  
Seol-Heui Han ◽  
...  
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Saatheeyavaane Bhuvanendran ◽  
Siti Najmi Syuhadaa Bakar ◽  
Yatinesh Kumari ◽  
Iekhsan Othman ◽  
Mohd. Farooq Shaikh ◽  
...  

Abstract Alzheimer’s disease (AD) is the second most occurring neurological disorder after stroke and is associated with cerebral hypoperfusion, possibly contributing to cognitive impairment. In the present study, neuroprotective and anti-AD effects of embelin were evaluated in chronic cerebral hypoperfusion (CCH) rat model using permanent bilateral common carotid artery occlusion (BCCAO) method. Rats were administered with embelin at doses of 0.3, 0.6 or 1.2 mg/kg (i.p) on day 14 post-surgery and tested in Morris water maze (MWM) followed by electrophysiological recordings to access cognitive abilities and synaptic plasticity. The hippocampal brain regions were extracted for gene expression and neurotransmitters analysis. Treatment with embelin at the doses of 0.3 and 0.6 mg/kg significantly reversed the spatial memory impairment induced by CCH in rats. Embelin treatment has significantly protected synaptic plasticity impairment as assessed by hippocampal long-term potentiation (LTP) test. The mechanism of this study demonstrated that embelin treatment alleviated the decreased expression of BDNF, CREB1, APP, Mapt, SOD1 and NFκB mRNA levels caused by CCH rats. Furthermore, treatment with embelin demonstrated neuromodulatory activity by its ability to restore hippocampal neurotransmitters. Overall these data suggest that embelin improve memory and synaptic plasticity impairment in CCH rats and can be a potential drug candidate for neurodegenerative disease-related cognitive disorders.


2020 ◽  
Vol 45 (11) ◽  
pp. 2631-2640
Author(s):  
Ashkan Divanbeigi ◽  
Mohammad Nasehi ◽  
Salar Vaseghi ◽  
Sepideh Amiri ◽  
Mohammad-Reza Zarrindast

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Peipei Feng ◽  
Zemin Wu ◽  
Hao Liu ◽  
Yafang Shen ◽  
Xu Yao ◽  
...  

Electroacupuncture (EA) can effectively alleviate anxiety disorders and memory impairments caused by various neurodegenerative diseases; however, the molecular mechanisms underlying its neuroprotective effects are unclear. Previous studies have shown that the renin-angiotensin system (RAS) comprises of two axes with mutual antagonism: the classical angiotensin converting enzyme/angiotensin II/angiotensin II type 1 receptor (ACE/Ang II/AT1R) axis and the protective angiotensin converting enzyme 2/angiotensin-(1-7)/Mas receptor (ACE2/Ang-(1-7)/MasR) axis. In this study, we observed that chronic cerebral hypoperfusion (CCH) mediated anxiety-like behavior and memory impairments in spontaneously hypertensive rats (SHR) via upregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and the partial hippocampal protective axis (ACE2/Ang-(1-7)). However, Ang II levels were much higher than those of Ang-(1–7), indicating that the ACE/Ang II/AT1R axis plays a dominant role in the comorbidity of CCH and hypertension. Moreover, candesartan cilexetil (Canc) and perindopril (Peril) were used as positive control drugs. We found that EA, Canc, and Peril attenuated CCH-induced anxiety-like behavior and memory impairments in SHR, potentially via downregulation of the hippocampal classical axis (ACE/Ang II/AT1R) and upregulation of the whole hippocampal protective axis (ACE2/Ang-(1-7)/MasR). These results suggest that EA therapy for CCH with hypertension may be mediated by two hippocampal RAS axes.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ling-Yong Xiao ◽  
Jing-Wen Yang ◽  
Xue-Rui Wang ◽  
Yang Ye ◽  
Na-Na Yang ◽  
...  

Alteration of dopamine (DA) and noradrenaline (NA) contributes to cognitive function. Acupuncture has been shown to affect DA and NA in chronic cerebral hypoperfusion (CCH) rats. However, the effect of acupuncture on DA-β-hydroxylase (DBH), the biosynthetic enzyme of NA, remains unknown. In CCH rats we established chronic hypoperfusion by bilateral common carotid artery occlusion (two-vessel occlusion, 2VO) and treated them with acupuncture. Acupuncture displayed beneficial effects on hippocampus-dependent memory impairments, including nonspatial and spatial memory. That is also reflected in hippocampus long-term-potentiation (LTP). Moreover, DBH expression in the hippocampus and DBH activity in cerebrospinal fluid were upregulated after acupuncture treatment. In conclusion, these in vivo findings suggest that acupuncture exerts a therapeutic effect on hippocampus-dependent memory and hippocampus LTP in CCH rats, which may be partially related to the modulation of DBH in the hippocampus.


2021 ◽  
Vol 12 ◽  
Author(s):  
Miao Zhang ◽  
Yuan Hu ◽  
Jiahui Zhang ◽  
Junjian Zhang

Vascular dementia (VD) and Alzheimer's disease (AD) are the most prevalent types of late-life dementia. Chronic cerebral hypoperfusion (CCH) contributes to both AD and VD. Recently, accumulating evidence has indicated that fingolimod (FTY720) is neuroprotective in acute cerebral ischemic stroke animal models, and the drug is now being used in clinical translation studies. However, fewer studies have addressed the role of FTY720 in chronic cerebral hypoperfusion (CCH)-related brain damage. In the present study, to investigate whether FTY720 can improve CCH-induced spatial memory loss and its underlying mechanism, two-vessel occlusion (2VO) rats were administered intraperitoneal FTY720 (1 mg/kg) for 7 consecutive weeks from post-operative day 8. Spatial memory was tested using the Morris Water Maze (MWM), and the rats' brains were harvested to allow molecular, biochemical, and pathological tests. We found that FTY720 treatment significantly reduced the escape latency and increased the target quadrant swimming time of the 2VO rats in the MWM task. The improvement in memory performance paralleled lower levels of pro-inflammatory cytokines and Iba-1 positive cells in the hippocampus of the 2VO rats, indicating that FTY720 had a beneficial effect in mitigating neuroinflammation. Furthermore, we found that FTY720 alleviated mitochondrial dysfunction in 2VO rats, as manifested by lower malondialdehyde levels, higher ATP content, and upregulation of ATP synthase activity in the hippocampus after treatment. FTY720 had no effect on the CCH-induced decrease in the activity of hippocampal Sirtuin-3, a master regulator of mitochondrial function and neuroinflammation. In summary, the results showed that FTY720 can improve CCH-induced spatial memory loss. The mechanism may involve Sirtuin-3-independent regulation of mitochondrial dysfunction and neuroinflammation in the hippocampus. The present study provides new clues to the pathological mechanism of CCH-induced cognitive impairment.


2018 ◽  
Vol 63 (2) ◽  
pp. 445-455 ◽  
Author(s):  
Chen Chen ◽  
Haifeng Zhang ◽  
Hongliang Xu ◽  
Rui Xue ◽  
Yake Zheng ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Won Kyung Jeon ◽  
Jinhua Ma ◽  
Bo-Ryoung Choi ◽  
Seol-Heui Han ◽  
Qinghao Jin ◽  
...  

Fructus mume(F. mume) has been used as a medicinal food in Japan and has been reported to have anti-inflammatory effects in inflammatory bowel disease and macrophage-mediated inflammation. We investigated the effects ofF. mumeextracts on cognitive dysfunction in rats with chronic cerebral hypoperfusion and the molecular mechanisms underlying these effects. Chronic cerebral hypoperfusion was induced in male Wister rats by bilateral common artery occlusion (BCCAo). Daily administration ofF. mumeextracts was started on day 20 after post-BCCAo and continued for 40 days. The status of hippocampus-dependent memory was evaluated in control rats, rats with chronic cerebral hypoperfusion, and rats with chronic cerebral hypoperfusion that were administeredF. mume. The levels of microglial activation were measured in the hippocampus and the fimbria of hippocampus, and expression levels of hippocampal mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) were examined. Rats that received chronic cerebral hypoperfusion showed spatial memory impairments relative to the control rats; these impairments were reduced by daily administration ofF. mume. Administration ofF. mumemitigated the microglial activation and alterations of hippocampal MAPK and NF-κB signaling in the rats with chronic cerebral hypoperfusion. These results indicate thatF. mumemay possess therapeutic potential for the prevention of vascular dementia via inhibition of inflammatory processes.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Min-Soo Kim ◽  
Won Kyung Jeon ◽  
Kye Wan Lee ◽  
Yu Hwa Park ◽  
Jung-Soo Han

We previously reported thatFructus mume(F. mume) extract shows protective effects on memory impairments and anti-inflammatory effects induced by chronic cerebral hypoperfusion. Neurodegeneration of basal cholinergic neurons is also observed in the brain with chronic cerebral hypoperfusion. Therefore, the present study was conducted to examine whetherF. mumeextracts enhance cognitive function via the action of cholinergic neuron using a scopolamine-induced animal model of memory impairments.F. mume(50, 100, or 200 mg/kg) was administered to C57BL/6 mice for 14 days (days 1–14) and memory impairment was induced by scopolamine (1 mg/kg), a muscarinic receptor antagonist for 7 days (days 8–14). Spatial memory was assessed using Morris water maze and hippocampal level of acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) was examined by ELISA and immunoblotting. Mice that received scopolamine alone showed impairments in acquisition and retention in Morris water maze task and increased activity of AChE in the hippocampus. Mice that receivedF. mumeand scopolamine showed no scopolamine-induced memory impairment and increased activity of AChE. In addition, treatments ofF. mumeincreased ChAT expression in the hippocampus. These results indicated thatF. mumemight enhance cognitive function via action of cholinergic neurons.


Sign in / Sign up

Export Citation Format

Share Document