Acupuncture Improves Cognitive Deficits and Increases Neuron Density of the Hippocampus in Middle-Aged Samp8 Mice

2012 ◽  
Vol 30 (4) ◽  
pp. 339-345 ◽  
Author(s):  
Guomin Li ◽  
Xuezhu Zhang ◽  
Haiyan Cheng ◽  
Xuemei Shang ◽  
Hui Xie ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Morris Water Maze ◽  
Cognitive Deficits ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Neuron Loss ◽  
Neuron Density ◽  
Maze Test ◽  
Samp8 Mice

Objectives To examine whether acupuncture could improve cognitive deficits and reduce the loss of neurons in mice models of ageing. Methods Male 7.5-month-old senescence-accelerated mouse prone 8 (SAMP8) and age-matched senescence-resistant inbred strains 1 (SAMR1) were divided into four groups (n=15 per group): SAMP8 acupuncture group (Pa), SAMP8 non-acupuncture point control group (Pn), SAMP8 control group (Pc) and SAMR1 normal control group (Rc). The behaviours were examined by the Morris water maze test and the neuron density in the hippocampus was estimated by the optical fractionator technique. Results The Morris water maze test demonstrated that the cognitive deficits of SAMP8 mice were improved by acupuncture treatment. Neuronal loss was found in hippocampal regions CA1 (−24%), CA3 (−18%) and DG (−28%) of Pc compared with Rc. The neuron number in hippocampal CA3 and DG of the Pa group was significantly increased by therapeutic acupuncture compared with the Pc group. Conclusions Acupuncture improved the cognitive impairment of middle-aged SAMP8 mice which could be attributed to the reduced neuron loss in hippocampal regions CA3 and DG. These results suggest that reducing neuron loss in the hippocampus by acupuncture is a potential therapeutic approach for the treatment of Alzheimer's disease and cognitive impairment diseases.

scholarly journals Musical Electroacupuncture May Be a Better Choice than Electroacupuncture in a Mouse Model of Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Jiang ◽  
Gang Liu ◽  
Suhua Shi ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Frontal Lobe ◽  
Morris Water Maze ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Model Of Alzheimer’S Disease ◽  
Samp8 Mice

Objectives. To compare musical electroacupuncture and electroacupuncture in a mouse model of Alzheimer’s disease.Methods. In this study, 7.5-month-old male senescence-accelerated mouse prone 8 (SAMP8) mice were used as an Alzheimer’s disease animal model. In the normal control paradigm, 7.5-month-old male SAMR1 mice were used as the blank control group (N group). After 15 days of treatment, using Morris water maze test, micro-PET, and immunohistochemistry, the differences among the musical electroacupuncture (MEA), electroacupuncture (EA), Alzheimer’s disease (AD), and normal (N) groups were assessed.Results. The Morris water maze test, micro-PET, and immunohistochemistry revealed that MEA and EA therapies could improve spatial learning and memory ability, glucose metabolism level in the brain, and Aβamyloid content in the frontal lobe, compared with the AD group (P<0.05). Moreover, MEA therapy performed better than EA treatment in decreasing amyloid-beta levels in the frontal lobe of mice with AD.Conclusion. MEA therapy may be superior to EA in treating Alzheimer’s disease as demonstrated in SAMP8 mice.

Ellagic Acid Administration Negated the Development of Streptozotocin-Induced Memory Deficit in Rats

Drug Research ◽  
2017 ◽  
Vol 67 (07) ◽  
pp. 425-431 ◽  
Author(s):  
Nitin Bansal ◽  
Pushplata Yadav ◽  
Manish Kumar
Keyword(s):  
Morris Water Maze ◽  
Cognitive Deficits ◽  
Ellagic Acid ◽  
Water Maze ◽  
Elevated Plus Maze ◽  
Morris Water Maze Test ◽  
Elevated Plus Maze Test ◽  
Maze Test ◽  
Tnf Α ◽  
Plus Maze

AbstractRampant production of pro-oxidants and inadequate antioxidant availability in brain exert oxidative stress, which in synergism with impaired glucose metabolism and inflammation leads to neurodegeneration and cognitive deficits. Ellagic acid (EGA) is a phenolic compound present in various fruits and is reported to possess robust antioxidant and anti-inflammatory properties. The present study investigated the effect of EGA administration on streptozotocin (STZ) induced dementia in rats. Bilateral intracerebroventricle (ICV) injection of STZ (3 mg/kg) was given to Wistar rats (200 g) on day 1 and 3. EGA (17.5 and 35 mg/kg) was administered orally to rats for 28 days daily. The spatial memory of rats was quantified by using Morris water maze and elevated plus maze. Brain TBARS, GSH and TNF-α were also measured. Administration of EGA prevented the induction of STZ-ICV triggered cognitive deficits as evident by a significant (p<0.05) reduction in mean escape latency during acquisition trial and increased (p<0.05) time spent in target quadrant during retrieval trial in Morris water maze test, and reduction (p<0.05) in transfer latency in elevated plus maze test. Furthermore, both the doses of EGA attenuated STZ-ICV induced rise in brain TBARS as well as TNF-α and simultaneously enhanced the GSH content. Thus, EGA ameliorated STZ-induced dementia by probably restoring the balance between cellular pro-oxidants and anti-oxidants in brain of rats.

scholarly journals Dimethyl fumarate prevents acute lung injury related cognitive impairment potentially via reducing inflammation

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Xiaowei Wang ◽  
Yanbo Wang ◽  
Haiyan Pan ◽  
Ci Yan
Keyword(s):  
Cognitive Impairment ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Water Maze ◽  
Dimethyl Fumarate ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Maze Test ◽  
Evans Blue Extravasation ◽  
Brain Tissues

Abstract Objective Dimethyl fumarate (DMF) has been reported to exert a protective role against diverse lung diseases and cognitive impairment-related diseases. Thus this study aimed to investigate its role on acute lung injury (ALI) and related cognitive impairment in animal model. Methods C57BL/6 mice were divided into four groups: control group, DMF group, ALI group, and ALI + DMF group. For ALI group, the ALI mice model was created by airway injection of LPS (50 μL, 1 μg/μL); for ALI + DMF group, DMF (dissolved in 0.08% methylcellulose) was treated twice a day for 2 days, and on the third day, mice were injected with LPS for ALI modeling. Mice pre-administered with methylcellulose or DMF without LPS injection (PBS instead) were used as the control group and DMF group, respectively. Morris water maze test was performed before any treatment (0 h) and 6 h after LPS-induction (54 h) to evaluate the cognitive impairment of mice. Next, the brain edema and blood brain barrier (BBB) permeability of ALI mice were assessed by brain water content, Evans blue extravasation and FITC-Dextran uptake assays. In addition, the effect of DMF on the numbers of total cells and neutrophils, protein content in BALF were quantified; the inflammatory factors in BALF, serum, and brain tissues were examined by ELISA, qRT-PCR, and Western blot assays. The effect of DMF on the cognitive impairment-related factor HIF-1α level in lung and brain tissues was also examined by Western blot. Results DMF reduced the numbers of total cells, neutrophils and protein content in BALF of ALI mice, inhibited the levels of IL-6, TNF-α and IL-1β in BALF, serum and brain tissues of ALI mice. The protein expressions of p-NF-κB/NF-κB and p-IKBα/IKBα was also suppressed by DMF in ALI mice. Morris water maze test showed that DMF alleviated the cognitive impairment in ALI mice by reducing the escape latency and path length. Moreover, DMF lessened the BBB permeability by decreasing cerebral water content, Evans blue extravasation and FITC-Dextran uptake in ALI mice. The HIF-1α levels in lung and brain tissues of ALI mice were also lessened by DMF. Conclusion In conclusion, DME had the ability to alleviate the lung injury and cerebral cognitive impairment in ALI model mice. This protective effect partly associated with the suppression of inflammation by DMF.

scholarly journals Effect of Nyctanthes arbor tristis leaf extract against scopolamine-induced cognitive impairment in rats

2015 ◽  
Vol 60 (4) ◽  
pp. 34-49
Author(s):  
Bashetty Phanindhra ◽  
Akondi Butchi Raju ◽  
Gadiyaram Vikas ◽  
Repala Anusha ◽  
Donapati Deepika
Keyword(s):  
Cognitive Impairment ◽  
Protective Effect ◽  
Morris Water Maze ◽  
Water Maze ◽  
Active Avoidance ◽  
Ethanol Extract ◽  
Thiobarbituric Acid ◽  
Morris Water Maze Test ◽  
Radial Arm Maze ◽  
Maze Test

Summary Nyctanthes arbor tristis (NATE) ethanol extract (150 mg/kg, orally) was evaluated for its protective effect against scopolamine-induced (1 mg/kg i.p.) cognitive impairments in rats using behavioral models like radial arm maze test, Morris water maze test and active avoidance test. NATE effect was evaluated and compared with the standard piracetam (200mg/kg i.p.). NATE (p<0.005) significantly reversed the impairment produced by the scopolamine in radial arm maze test. In addition, NATE also decreased the time period taken to find the hidden platform in Morris water maze test and increased number of avoidances in active avoidance paradigm. Acetylcholinesterase activity and thiobarbituric acid levels were significantly (p<0.005) decreased along with the rise in activities of superoxide dismutase and catalase. This might suggest that the NATE has protective effect against scopolamine-induced cognitive impairment in rats through acetylcholine muscarinic receptor pathway and also antioxidant activity. No significant changes were found in histopathological studies of brain.

Yam (Dioscorea pseudojaponica Yamamoto) Ameliorates Cognition Deficit and Attenuates Oxidative Damage in Senescent Mice Induced by D-Galactose

2009 ◽  
Vol 37 (05) ◽  
pp. 889-902 ◽  
Author(s):  
Chuan-Sung Chiu ◽  
Jeng-Shyan Deng ◽  
Ming-Tsuen Hsieh ◽  
Ming-Jen Fan ◽  
Min-Min Lee ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Cognitive Impairment ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Mice Brain ◽  
Endogenous Antioxidant

This study attempted to access the neuroprotective effect of yam (Dioscorea pseudojaponica Yamamoto) on the senescent mice induced by D-gal. The mice in the experiments were administered orally with yam (20, 100 or 500 mg/kg for 4 weeks, from the sixth week). The learning and memory abilities of the mice in Morris water maze test and the mechanisms involved in the neuroprotective effect of yam on the mice brain tissue were investigated. The content of diosgenin in the yam was also detected by using HPLC. Mice treated with yam were found to significantly improve their learning and memory abilities in Morris water maze test compared to those treated with D-gal (200 mg/kg for 10 weeks). In addition, yam was also found to increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and decrease the malondialdehyde (MDA) level on the brains of D-gal treated mice. Finally, the amount of diosgenin in the yam was 5.49 mg/g extract. To sum up, these results indicate that yam had the potential to be a useful treatment for cognitive impairment in TCM. Its beneficial effect may be partly mediated via enhancing endogenous antioxidant enzymatic activities.

scholarly journals Impact of amitriptyline on learning and memory

2021 ◽  
Vol 5 (1) ◽  
pp. 009-015
Author(s):  
CC Mfem ◽  
SA Seriki
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Acquisition Trial ◽  
Water Maze ◽  
Treated Group ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Maze Test ◽  
Significant Difference ◽  
Retention Trial

Background/aim: Amitriptyline belongs to class of known as tricycline antidepresant (TCA) that is being used to treat anxiety and depressive states. It may help improve mood and feelings of well-being, relieve anxiety and tension, help to improve sleep and increase energy level. The study investigated the effect of amitriptyline on learning and memory using eighteen (18) healthy Swiss mice of both sexes weighing 16 – 25 g. Method: The animals were divided into three (3) groups consisting of six (6) animals each. Group 1 served as the control group, Group 2 was administered with amitriptyline at a dose of 3 mg/kg body weight dissolved in 3 mls of distilled water, and used to test for learning, while Group three was also given similar administration like Group 2, but used to test for memory. All the animals were tested for learning and memory performance using Novel object recognition task and Morris water maze test. Results: The results obtained from the Novel object recognition task showed that there was a significant decrease (p < 0.05) in total object approach in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant decrease (p < 0.05) in retention trial of amitriptyline group when compared to retention trial in the control group. There was a significant decrease (p < 0.05) in total duration exploring objects in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant increase (p < 0.05) in total duration exploring objects in retention trial of amitriptyline treated group when compared to the retention trial of the control group. There was a significant decrease (p < 0.05) in the index of habituation of amitriptyline treated group when compared to the control group. The index of discrimination showed a significant increase (p < 0.05) in amitriptyline treated group when compared to the control group and a significant decrease (p < 0.05) in amitriptyline group when compared to the control group. In the Morris water maze test, Day 1 – 3 were for acquisition training, day 4 – 6 reversal training, day 7 the probe trial day and day 8 the visible platform day. During acquisition training in the Morris water maze test, there was no significant difference in Swim latencies in day 1 and 2. However in day 3, there was a significant increase (p < 0.05) in swim latency of group compared to control group and a significant decrease (p < 0.05) in swim latency of amitriptyline treated group compared to the control group. During reversal training in day 1, 2 and 3, there was no significant difference in swim latency among the three groups. Results for the retention quadrant in the probe trials showed a significant decrease (p < 0.01) in amitriptyline group when compared to the control group. Conclusion: Results suggest that amitriptyline impairs learning and memory functions.

Isoflurane-induced miR-140-5p aggravates neurotoxicity in diabetic rats by targeting SNX12

2019 ◽  
Vol 16 ◽  
Author(s):  
Dongyi Fan ◽  
Simin Yang ◽  
Yuxiang Han ◽  
Ru Zhang ◽  
Lukun Yang
Keyword(s):  
Cognitive Impairment ◽  
Morris Water Maze ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Diabetic Rats ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Luciferase Activity Assay ◽  
Novel Target ◽  
Isoflurane Treatment

Objectives: MicroRNAs (miRNAs) are widely known as critical regulators in isoflurane-induced neurotoxicity during the development of brain. Isoflurane could aggravate cognitive impairment in diabetic rats. The present study was designed to explore the role and mechanism of miR-140-5p on isoflurane-induced neurotoxicity in diabetic rats. Methods: Diabetic rats model was established by injection of streptozotocin (STZ) and identified by Morris water maze test. Expression of miR-140-5p in diabetic rats under isoflurane treatment was evaluated via qRT-PCR (quantitative real-time polymerase chain reaction). Latency to platform and time spent in the target quadrant were calculated to detect the effect of miR-140-5p on neurotoxicity. The potential target for miR-140-5p was validated via dual luciferase activity assay. Results: Morris water maze test indicated that isoflurane treatment exacerbated STZ-induced cognitive impairment, as demonstrated by increase of latency to platform and decrease of time spent in the target quadrant. MiR-140-5p was up-regulated in diabetic rats under isoflurane treatment. Moreover, knockdown of miR-140-5p attenuated neurotoxicity in diabetic rats. Mechanistically, we found that miR-140-5p could directly bind to SNX12 (sorting nexin 12). The neuroprotective effect of miR-140-5p against isoflurane-aggravated neurotoxicity in diabetic rats dependent on up-regulation of SNX12 and inhibition of cell apoptosis. Conclusions: Knockdown of miR-140-5p relieved isoflurane-aggravated neurotoxicity in diabetic rats through targeting SNX12, suggesting a novel target for neuroprotection in diabetes under isoflurane treatment.

Improvement of Impaired Memory in Mice by Schisandrin

2013 ◽  
Vol 750-752 ◽  
pp. 1533-1538
Author(s):  
Yan Chun Wang ◽  
Kuang Ren ◽  
Nan Shen ◽  
Xiao Dong Huang ◽  
Hong Yan Fan
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Cellular Response ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Tissue Samples ◽  
Pentobarbital Sodium ◽  
Maze Test

We assessed the effectiveness and mechanism of action of schisandrin on modulation of learning and memory disorders in mice. Memory impairment was established in mice by intraperitoneal injection of pentobarbital sodium (20 mg/kg). Schisandrin (0.5, 1.0, 2.0g/kg) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of schisandrin to reduce phenobarbital-induced learning and memory impairment. The levels of superoxide dismutase (SOD) nitric oxide (NO) and catalase (CAT) were measured in brain tissue samples taken from the mice. Other biomarkers measured included expression of nuclear transcription factor-kappa-B (NF-κB) and brain-derived neurotrophic factor (BDNF) in the hippocampus CA1 region, which were determined by immunohistochemical analysis. On the fifth day of treatment, the mice in the pentobarbital sodium group performed worse on the Morris water maze test compared to untreated controls (P<0.01), which could be prolonged after schisandrin treatment (P<0.05 for="" low="" and="" intermediate="" dose="" groups="" analysis="" of="" brain="" tissues="" showed="" that="" compared="" with="" the="" control="" group="" no="" levels="" were="" increased="" sod="" cat="" activity="" decreased="" in="" pentobarbital="" sodium="" i="">P<0.01). After treatment with schisandrin, the NO levels were significantly decreased (P<0.01), while SOD and CAT activity increased (P<0.01). Immunohistochemistry analysis showed that, in phenobarbital only group, the protein expression of BDNF decreased, NF-κB increased compared to untreated controls, and schisandrin could reverse this trend (P<0.05 and="" i="">P<0.01, respectively). The results suggest that schisandrin is effective in improving the learning and memory deficiency induced by pentobarbital sodium, the mechanism of which may be related modulation of cellular response to oxidative stress.

scholarly journals Indoleamine 2,3-Dioxygenase-Dependent Neurotoxic Kynurenine Metabolism Contributes to Poststroke Depression Induced in Mice by Ischemic Stroke along with Spatial Restraint Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Young Soo Koo ◽  
Hyunha Kim ◽  
Jung Hwa Park ◽  
Min Jae Kim ◽  
Yong-Il Shin ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Nucleus Accumbens ◽  
Morris Water Maze ◽  
Water Maze ◽  
Restraint Stress ◽  
Sucrose Preference ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Ido1 Expression ◽  
Kynurenine Metabolism

Aim. Poststroke depression (PSD), which occurs in approximately one-third of stroke survivors, is clinically important because of its association with slow functional recovery and increased mortality. In addition, the underlying pathophysiological mechanisms are still poorly understood. Methods. We used a mouse model of PSD to examine the neurobiological mechanisms of PSD and the beneficial effects of aripiprazole, an atypical antipsychotic drug. PSD was induced in mice by combining middle cerebral artery occlusion (MCAO) with spatial restraint stress. The body weight, sucrose preference, and forced swim tests were performed at 5, 7, and 9 weeks and the Morris water maze test at 10 weeks after completing MCAO and spatial restraint stress. Results. Mice subjected to MCAO and spatial restraint stress showed significant depressive-like behavior in the sucrose preference test and forced swim test as well as cognitive impairment in the Morris water maze test. The PSD-like phenotype was accompanied by an indoleamine 2,3-dioxygenase 1 (IDO1) expression increase in the nucleus accumbens, hippocampus, and hypothalamus, but not in the striatum. Furthermore, the increased IDO1 levels were localized in Iba-1(+) cells but not in NeuN(+) or GFAP(+) cells, indicating that microglia-induced IDO1 expression was prominent in the PSD mouse brain. Moreover, 3-hydroxyanthranilate 3,4-dioxygenase (HAAO), quinolinic acid (QUIN), and reactive oxygen species (ROS) were significantly increased in the nucleus accumbens, hippocampus, and hypothalamus of PSD mice. Importantly, a 2-week aripiprazole (1 mg/kg, per os) regimen, which was initiated 1 day after MCAO, ameliorated depressive-like behavior and impairment of cognitive functions in PSD mice that was accompanied by downregulation of IDO1, HAAO, QUIN, and ROS. Conclusions. Our results suggest that the IDO1-dependent neurotoxic kynurenine metabolism induced by microglia functions in PSD pathogenesis. The beneficial effect of aripiprazole on depressive-like behavior and cognitive impairment may be mediated by inhibition of IDO1, HAAO, QUIN, and ROS.

Protective Effects of Dendrobium nobile Lindl. Alkaloids on Alzheimer's Disease-like Symptoms Induced by High-methionine Diet

2021 ◽  
Vol 19 ◽  
Author(s):  
Tingting Pi ◽  
Guangping Lang ◽  
Bo Liu ◽  
Jingshan Shi
Keyword(s):  
Alzheimer’S Disease ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Cpg Island ◽  
Morris Water Maze Test ◽  
Dendrobium Nobile ◽  
Maze Test ◽  
Neuron Damage ◽  
Cpg Island Methylation

Background: High methionine-diet (HMD) causes Alzheimer's disease (AD)-like symptoms. Previous studies have shown that Dendrobium nobile Lindle. alkaloids (DNLA) had potential benefits for AD. Object: Whether DNLA can improve AD-like symptoms induced by HMD is to be explored. Method: Mice were fed with 2% HMD diet for 11 weeks, the DNLA20 control group (20 mg/kg), DNLA10 group (10 mg/kg), and DNLA20 group (20 mg/kg) were administrated with DNLA for 3 months. Morris water maze test was used to detect learning and memory ability. Neuron damage was evaluated by HE and Nissl stainings. Levels of homocysteine (Hcy), beta-amyloid 1-42 (Aβ1-42), S-adenosine methionine (SAM), and S-adenosine homocysteine (SAH) were detected by ELISA. Immunofluorescence and western blotting (WB) were used to determine the expression of proteins. CPG island methylation. Results: Morris water maze test revealed that DNLA improved learning and memory dysfunction. HE, Nissl, and immunofluorescence stainings showed that DNLA alleviated neuron damage and reduced the 5-methylcytosine (5-mC), Aβ1-40, and Aβ1-42 levels. DNLA also decreased the levels of Hcy and Aβ1-42 in the serum, along with decreased SAM/SAH levels in the liver tissue. WB results showed that DNLA down-regulated the expression of the amyloid-precursor protein (APP), presenilin-1 (PS1), beta-secretase-1 (BACE1), DNA methyltransferase1 (DNMT1), Aβ1-40, and Aβ1-42 proteins. DNLA also up-regulated the expression of the protein of insulin-degrading enzyme (IDE), neprilysin (NEP), DNMT3a, and DNMT3b. Meanwhile, DNLA increased CPG island methylation levels of APP and BACE1 genes. Conclusions: DNLA alleviated AD-like symptoms induced by HMD via the DNA methylation pathway.

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