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Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism 被引量:3
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作者 Jie Li Wen Jiang +9 位作者 Yuefang Cai Zhenqiu Ning Yingying Zhou Chengyi Wang Sookja Ki Chung Yan Huang Jingbo Sun Minzhen Deng Lihua Zhou Xiao Cheng 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期650-656,共7页
Vascular etiology is the second most prevalent cause of cognitive impairment globally.Endothelin-1,which is produced and secreted by endothelial cells and astrocytes,is implicated in the pathogenesis of stroke.However... Vascular etiology is the second most prevalent cause of cognitive impairment globally.Endothelin-1,which is produced and secreted by endothelial cells and astrocytes,is implicated in the pathogenesis of stroke.However,the way in which changes in astrocytic endothelin-1 lead to poststroke cognitive deficits following transient middle cerebral artery occlusion is not well understood.Here,using mice in which astrocytic endothelin-1 was overexpressed,we found that the selective overexpression of endothelin-1 by astrocytic cells led to ischemic stroke-related dementia(1 hour of ischemia;7 days,28 days,or 3 months of reperfusion).We also revealed that astrocytic endothelin-1 overexpression contributed to the role of neural stem cell proliferation but impaired neurogenesis in the dentate gyrus of the hippocampus after middle cerebral artery occlusion.Comprehensive proteome profiles and western blot analysis confirmed that levels of glial fibrillary acidic protein and peroxiredoxin 6,which were differentially expressed in the brain,were significantly increased in mice with astrocytic endothelin-1 overexpression in comparison with wild-type mice 28 days after ischemic stroke.Moreover,the levels of the enriched differentially expressed proteins were closely related to lipid metabolism,as indicated by Kyoto Encyclopedia of Genes and Genomes pathway analysis.Liquid chromatography-mass spectrometry nontargeted metabolite profiling of brain tissues showed that astrocytic endothelin-1 overexpression altered lipid metabolism products such as glycerol phosphatidylcholine,sphingomyelin,and phosphatidic acid.Overall,this study demonstrates that astrocytic endothelin-1 overexpression can impair hippocampal neurogenesis and that it is correlated with lipid metabolism in poststroke cognitive dysfunction. 展开更多
关键词 astrocytic endothelin-1 dentate gyrus differentially expressed proteins HIPPOCAMPUS ischemic stroke learning and memory deficits lipid metabolism neural stem cells NEUROGENESIS proliferation
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Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice
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作者 Yujia Liu Xue Han +6 位作者 Yan Su Yiming Zhou Minhui Xu Jiyan Xu Zhengliang Ma Xiaoping Gu Tianjiao Xia 《Neural Regeneration Research》 SCIE CAS 2025年第9期2727-2736,共10页
Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life ... Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction. 展开更多
关键词 Chil1 hippocampus learning and memory M2 microglia NEUROINFLAMMATION postoperative cognitive dysfunction(POCD) recombinant CHI3L1
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Mechanism of Learning and Memory Impairment in Rats Exposed to Arsenic and/or Fluoride Based on Microbiome and Metabolome 被引量:3
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作者 ZHANG Xiao Li YU Sheng Nan +12 位作者 QU Ruo Di ZHAO Qiu Yi PAN Wei Zhe CHEN Xu Shen ZHANG Qian LIU Yan LI Jia GAO Yi LYU Yi YAN Xiao Yan LI Ben REN Xue Feng QIU Yu Lan 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2023年第3期253-268,共16页
Objective Arsenic(As) and fluoride(F) are two of the most common elements contaminating groundwater resources. A growing number of studies have found that As and F can cause neurotoxicity in infants and children, lead... Objective Arsenic(As) and fluoride(F) are two of the most common elements contaminating groundwater resources. A growing number of studies have found that As and F can cause neurotoxicity in infants and children, leading to cognitive, learning, and memory impairments. However, early biomarkers of learning and memory impairment induced by As and/or F remain unclear. In the present study, the mechanisms by which As and/or F cause learning memory impairment are explored at the multi-omics level(microbiome and metabolome).Methods We stablished an SD rats model exposed to arsenic and/or fluoride from intrauterine to adult period.Results Arsenic and/fluoride exposed groups showed reduced neurobehavioral performance and lesions in the hippocampal CA1 region. 16S rRNA gene sequencing revealed that As and/or F exposure significantly altered the composition and diversity of the gut microbiome, featuring the Lachnospiraceae_NK4A136_group, Ruminococcus_1, Prevotellaceae_NK3B31_group, [Eubacterium]_xylanophilum_group. Metabolome analysis showed that As and/or F-induced learning and memory impairment may be related to tryptophan, lipoic acid, glutamate, gamma-aminobutyric acidergic(GABAergic) synapse, and arachidonic acid(AA) metabolism. The gut microbiota, metabolites, and learning memory indicators were significantly correlated.Conclusion Learning memory impairment triggered by As and/or F exposure may be mediated by different gut microbes and their associated metabolites. 展开更多
关键词 ARSENIC FLUORIDE learning and memory impairment MICROBIOME METABOLOME
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BI-D1870 Causes the Rats’ Learning and Memory Acquisition Ability Impairment 被引量:2
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作者 Chaojie Zhang Ke He +1 位作者 Caixia Li Yazhen Shang 《Journal of Biosciences and Medicines》 CAS 2023年第1期82-97,共16页
Aim: To observe the rats’ learning and memory acquisition ability disturbance induced by BI-D1870. Methods: Male SD rats were randomly divided into control group, solvent control group and BI-D1870 group. The rats in... Aim: To observe the rats’ learning and memory acquisition ability disturbance induced by BI-D1870. Methods: Male SD rats were randomly divided into control group, solvent control group and BI-D1870 group. The rats in the control group were intraperitoneally injected with saline, while those in the solvent control group were intraperitoneally injected with DMSO + sulfobutyl-β-cyclodextrin solvent, and those in the BI-D1870 group were intraperitoneally injected with BI-D1870. All the rats’ appearance and behavior were daily observed, and body weight was recorded on the day 15, 30, 45, 60, 75 and 82 of BI-D1870 injected. Morris water maze was used to screen the rats’ learning and memory acquisition ability on the day 22 - 25, 52 - 55, and 82 - 85 of training by BI-D1870 treated. The successful rates of the rats’ memory impairment were respectively calculated for three times screening. Results: During the whole experiment, there was no obvious difference in appearance and fur color in all rats. The rats’ agitation began to appear on the day 10th of BI-D1870 given. The agitation rats’ number and rats’ body weight gradually increased along with BI-D1870 treated (P P Conclusion: Intraperitoneal injection of BI-D1870 can induce the rats’ learning and memory acquisition ability disorder. 展开更多
关键词 BI-D1870 learning and memory Acquisition Impairment Morris Water Maze RSK Inhibitor
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Tree shrew models:A chronic social defeat model of depression and a one-trial captive conditioning model of learning and memory 被引量:21
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作者 王静 周启心 +2 位作者 田孟 杨跃雄 徐林 《Zoological Research》 CAS CSCD 北大核心 2011年第1期24-30,共7页
Recent genome studies indicate that tree shrew is in the order or a closest sister of primates,and thus may be one of the best animals to model human diseases.In this paper,we report on a social defeat model of depres... Recent genome studies indicate that tree shrew is in the order or a closest sister of primates,and thus may be one of the best animals to model human diseases.In this paper,we report on a social defeat model of depression in tree shrew(Tupaia belangeri chinensis).Two male tree shrews were housed in a pair-cage consisting of two independent cages separated by a wire mesh partition with a door connecting the two cages.After one week adaptation,the connecting door was opened and a brief fighting occurs between the two male tree shrews and this social conflict session consisted of 1 h direct conflict(fighting) and 23 h indirect influence(e.g.smell,visual cues) per day for 21 days.The defeated tree shrew was considered the subordinate.Compared with na?ve animals,subordinate tree shrews at the final week of social conflict session showed alterations in body weight,locomotion,avoidance behavior and urinary cortisol levels.Remarkably,these alterations persisted for over two weeks.We also report on a novel captive conditioning model of learning and memory in tree shrew.An automatic trapping cage was placed in a small closed room with a freely-moving tree shrew.For the first four trials,the tree shrew was not trapped when it entered the cage and ate the bait apple,but it was trapped and kept in the cage for 1 h on the fifth trial.Latency was defined as the time between release of the tree shrew and when it entered the captive cage.Latencies during the five trials indicated adaptation.A test trial 24 h later was used to measure whether the one-trial trapping during the fifth trial could form captive memory.Tree shrews showed much longer trapping latencies in the test trial than the adaptation trials.The N-methyl-d-aspartate(NMDA) receptor antagonist MK-801(0.2 mg/kg,i.p.),known to prevent the formation of memory,did not affect latencies in the adaptation trails,but did block captive memory as it led to much shorter trapping latencies compared to saline treatment in the test trial.These results demonstrate a chronic social defeat model of depression and a novel one-trial captive conditioning model for learning and memory in tree shrews,which are important for mechanism studies of depression,learning,memory,and preclinical evaluation for new antidepressants. 展开更多
关键词 Social defeat DEPRESSION Captive conditioning learning and memory Tree shrew
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Microglia regulation of synaptic plasticity and learning and memory 被引量:34
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作者 Jessica Cornell Shelbi Salinas +1 位作者 Hou-Yuan Huang Miou Zhou 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第4期705-716,共12页
Microglia are the resident macrophages of the central nervous system.Microglia possess varied morphologies and functions.Under normal physiological conditions,microglia mainly exist in a resting state and constantly m... Microglia are the resident macrophages of the central nervous system.Microglia possess varied morphologies and functions.Under normal physiological conditions,microglia mainly exist in a resting state and constantly monitor their microenvironment and survey neuronal and synaptic activity.Through the C1 q,C3 and CR3"Eat Me"and CD47 and SIRPα"Don't Eat Me"complement pathways,as well as other pathways such as CX3 CR1 signaling,resting microglia regulate synaptic pruning,a process crucial for the promotion of synapse formation and the regulation of neuronal activity and synaptic plasticity.By mediating synaptic pruning,resting microglia play an important role in the regulation of experience-dependent plasticity in the barrel cortex and visual cortex after whisker removal or monocular deprivation,and also in the regulation of learning and memory,including the modulation of memory strength,forgetfulness,and memory quality.As a response to brain injury,infection or neuroinflammation,microglia become activated and increase in number.Activated microglia change to an amoeboid shape,migrate to sites of inflammation and secrete proteins such as cytokines,chemokines and reactive oxygen species.These molecules released by microglia can lead to synaptic plasticity and learning and memory deficits associated with aging,Alzheimer's disease,traumatic brain injury,HIV-associated neurocognitive disorder,and other neurological or mental disorders such as autism,depression and post-traumatic stress disorder.With a focus mainly on recently published literature,here we reviewed the studies investigating the role of resting microglia in synaptic plasticity and learning and memory,as well as how activated microglia modulate disease-related plasticity and learning and memory deficits.By summarizing the function of microglia in these processes,we aim to provide an overview of microglia regulation of synaptic plasticity and learning and memory,and to discuss the possibility of microglia manipulation as a therapeutic to ameliorate cognitive deficits associated with aging,Alzheimer's disease,traumatic brain injury,HIV-associated neurocognitive disorder,and mental disorders. 展开更多
关键词 AGING Alzheimer's disease cognitive deficits experience-dependent plasticity learning and memory mental disorders MICROGLIA synaptic plasticity synaptic pruning
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Effects of exercise on neurogenesis in the dentate gyrus and ability of learning and memory after hippocampus lesion in adult rats 被引量:11
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作者 Lin CHEN Shan GONG +6 位作者 Li-Dong SHAN Wei-Ping XU Yue-Jin ZHANG Shi-Yu GUO Tadashi Hisamitsu Qi-Zhang YIN Xing-Hong JIANG 《Neuroscience Bulletin》 SCIE CAS CSCD 2006年第1期1-6,共6页
Objective To explore the effects of exercise on dentate gyrus (DG) neurogenesis and the ability of learning and memory in hippocampus-lesioned adult rats. Methods Hippocampus lesion was produced by intrabippocampal ... Objective To explore the effects of exercise on dentate gyrus (DG) neurogenesis and the ability of learning and memory in hippocampus-lesioned adult rats. Methods Hippocampus lesion was produced by intrabippocampal microinjection of kainic acid (KA). Bromodeoxyuridine (BrdU) was used to label dividing cells. Y maze test was used to evaluate the ability of learning and memory. Exercise was conducted in the form of forced running in a motor-driven running wheel. The speed of wheel revolution was regulated at 3 kinds of intensity: lightly running, moderately running, or heavily running. Results Hippocampus lesion could increase the number of BrdU-labeled DG cells, moderately running after lesion could further enhance the number of BrdU-labeled cells and decrease the error number (EN) in Y maze test, while neither lightly running, nor heavily running had such effects. There was a negative correlation between the number of DG BrdU-labeled cells and the EN in the Y maze test after running. Conclusion Moderate exercise could enhance the DG neurogenesis and ameliorate the ability of learning and memory in hippocampus-lesioned rats. 展开更多
关键词 NEUROGENESIS dentate gyms kainic acid learning and memory EXERCISE running BROMODEOXYURIDINE
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Eleutheroside B or E enhances learning and memory in experimentally aged rats 被引量:8
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作者 Debin Huang Zehua Hu Zhaofen Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第12期1103-1112,共10页
Eleutheroside B or E, the main component of Acanthopanax, can relieve fatigue, enhance memory, and improve human cognition. Numerous studies have confirmed that high doses of acetylcholine significantly attenuate clin... Eleutheroside B or E, the main component of Acanthopanax, can relieve fatigue, enhance memory, and improve human cognition. Numerous studies have confirmed that high doses of acetylcholine significantly attenuate clinical symptoms and delay the progression of Alzheimer's disease. The present study replicated a rat model of aging induced by injecting quinolinic acid into the hippocampal CA1 region. These rats were intraperitoneally injected with low, medium and high doses of eleutheroside B or E (50, 100, 200 mg/kg), and rats injected with Huperzine A or PBS were used as controls. At 4 weeks after administration, behavioral tests showed that the escape latencies and errors in searching for the platform in a Morris water maze were dose-dependently reduced in rats treated with medium and high-dose eleutheroside B or E. Hematoxylin-eosin staining showed that the number of surviving hippocampal neurons was greater and pathological injury was milder in three eleutheroside B or E groups compared with model group. Hippocampal homogenates showed enhanced cholinesterase activity, and dose-dependent increases in acetylcholine content and decreases in choline content following eleutheroside B or E treatment, similar to those seen in the Huperzine A group. These findings indicate that eleutheroside B or E improves learning and memory in aged rats. These effects of eleutheroside B or E may be mediated by activation of cholinesterase or enhanced reuse of choline to accelerate the synthesis of acetylcholine in hippocampal neurons. 展开更多
关键词 neural regeneration traditional Chinese medicine eleutheroside B or E quinolinic acid aged rats Huperzine A learning and memory HIPPOCAMPUS ACETYLCHOLINE CHOLINESTERASE CHOLINE mechanism grants-supported paper NEUROREGENERATION
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Effect of Panax notoginseng saponins on the expression of beta-amyloid protein in the cortex of the parietal lobe and hippocampus, and spatial learning and memory in a mouse model of senile dementia 被引量:9
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作者 Zhenguo Zhong Dengpan Wu Liang Lu Jinsheng Wang Wenyan Zhang Zeqiang Qu 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第12期1297-1303,共7页
BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheime... BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer's disease. OBJECTIVE: Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein (App) and β -amyloid (A β ), to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 (SAMP8) and compare the effects with huperzine A. DESIGN, TIME AND SETTING: A completely randomized grouping design, controlled animal experiment was performed in the Center for Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS: Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups: PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. (batch No.: Z53021485, Yuxi, Yunan Province, China). Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. (batch No.: 20040801, Zhejiang, China). METHODS: The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES: After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency (time-to-platform), and the percentage of swimming time spent in each quadrant. The number of A β 1-40, A β 1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content ofApp, tau, acetylcholinesterase, and synaptophysin (Syp) was tested by real time PCR and RT-PCR. RESULTS: The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group (P 〈 0.05). The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of A β 1-40, A β 1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group (P 〈 0.05). CONCLUSION: These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer's disease. The therapeutic effects of PNS for Alzheimer's disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A. 展开更多
关键词 Alzheimer's disease Panax notoginseng saponins learning and memory β -amyloid precursor protein 1-40 β -amyloid precursor protein 1-42 amyloid β -peptide SYNAPTOPHYSIN senescence accelerated mouse-prone 8
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Basic roles of key molecules connected with NMDAR signaling pathway on regulating learning and memory and synaptic plasticity 被引量:17
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作者 Hui Wang Rui-Yun Peng 《Journal of Medical Colleges of PLA(China)》 CAS 2016年第4期212-218,共7页
With key roles in essential brain functions ranging from the long-term potentiation(LTP) to synaptic plasticity,the N-methyl-D-aspartic acid receptor(NMDAR) can be considered as one of the fundamental glutamate recept... With key roles in essential brain functions ranging from the long-term potentiation(LTP) to synaptic plasticity,the N-methyl-D-aspartic acid receptor(NMDAR) can be considered as one of the fundamental glutamate receptors in the central nervous system.The role of NMDA R was first identified in synaptic plasticity and has been extensively studied.Some molecules,such as Ca^(2+),postsynaptic density 95(PSD-95),calcium/calmodulin-dependent protein kinase II(Ca MK II),protein kinase A(PKA),mitogen-activated protein kinase(MAPK) and cyclic adenosine monophosphate(c AMP) responsive element binding protein(CREB),are of special importance in learning and memory.This review mainly focused on the new research of key molecules connected with learning and memory,which played important roles in the NMDAR signaling pathway. 展开更多
关键词 N-methyl-D-aspartic acid receptors Long-term potentiation Synaptic plasticity learning and memory
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Radix Achyranthis Bidentatae improves learning and memory capabilities in ovariectomized rats 被引量:4
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作者 Yuefen Wang Ya Xu +5 位作者 Yanshu Pan Weihong Li Wei Zhang Yang Liu Jing Jia Pengtao Li 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第18期1644-1654,共11页
Kidney-tonifying recipe can reduce the accumulation of advanced glycation end products, prevent neuronal degeneration and improve cognitive functions in ovariectomized rats. Radix Achyranthis Bidentatae alcohol extrac... Kidney-tonifying recipe can reduce the accumulation of advanced glycation end products, prevent neuronal degeneration and improve cognitive functions in ovariectomized rats. Radix Achyranthis Bidentatae alcohol extracts may dose-dependently inhibit non-enzymatic saccharification in vitro. This study aimed to examine the effect of Radix Achyranthis Bidentatae on advanced glycation end products and on learning and memory capabilities in ovariectomized rats. Ovariectomized rats were treated with Radix Achyranthis Bidentatae alcohol extracts (containing 1.5 g/kg crude drug) or 0.1% aminoguanidine for 12 weeks and behavioral testing was performed with the Y-electrical maze. This test revealed that Radix Achyranthis Bidentatae and aminoguanidine could improve the learning and memory capabilities of ovariectomized rats. Results of competitive enzyme-linked immunosorbent assay showed that treatment with Radix Achyranthis Bidentatae or aminoguanidine reduced the accumulation of advanced glycation end products in the frontal cortex of ovariectomized rats, while increasing content in the blood and urine. Biochemical tests showed that treatment with Radix Achyranthis Bidentatae or aminoguanidine decreased superoxide dismutase activity in the serum and frontal cortex, and increased serum levels of glutathione peroxidase in ovariectomized rats. In addition there was no apparent effect on malondialdehyde levels. These experimental findings indicate that Radix Achyranthis Bidentatae inhibits production of advanced glycation end products and its accumulation in brain tissue, and improves learning and memory capabilities in ovariectomized rats. These effects may be associated with an anti-oxidative action of the extract. 展开更多
关键词 neural regeneration traditional Chinese medicine Alzheimer's disease Radix Achyranthis Bidentatae OVARIECTOMY advanced glycation end products COGNITION learning and memory oxidative stress grants-supported paper NEUROREGENERATION
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Impacts of Passive Smoking on Learning and Memory Ability of Mouse Offsprings and Intervention by Antioxidants 被引量:4
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作者 JIE YANG LI-NA JIANG +8 位作者 ZHEN-LI YUAN Yu-FEIZHENG Lu WANG MIN JI ZHI-QIANG SHEN XIN-WEI WANG QIANG MA ZHU-GE XI JUN-WEN LI 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2008年第2期144-149,共6页
Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pre... Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation (LTP). Nitric oxide (NO), content, nitric oxide synthase (NOS), acetylcholinesteras (Ache) activity in brain, vitamin E concentration, and reactive oxygen species (ROS) in serum were determined. The latency period (the time during which the mice swim from the starting position to the ending position) and errors (the number of mice entering the blind end) in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. Results The latency period as well as errors in the air, control diet, tobacco smoke (TS), and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups (P〈O.05). LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras (Ache) activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group (P〈0.05). Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. Conclusion Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS (especially vitamin E) partially improve the learning and memory smoke during pregnancy. and Ache activity and increasing NO content. Antioxidants ability of offsprings whose mothers are exposed to tobacco 展开更多
关键词 Passive smoking Mice offspring learning and memory ability Long term potentiation Antioxidant intervention
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Lithium chloride ameliorates learning and memory ability and inhibits glycogen synthase kinase-3 beta activity in a mouse model of fragile X syndrome 被引量:3
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作者 Shengqiang Chen Xuegang Luo +6 位作者 Quan Yang Weiwen Sun Kaiyi Cao Xi Chen Yueling Huang Lijun Dai Yonghong Yi 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第31期2452-2459,共8页
In the present study,Fmr1 knockout mice (KO mice) were used as the model for fragile X syndrome.The results of step-through and step-down tests demonstrated that Fmr1 KO mice had shorter latencies and more error cou... In the present study,Fmr1 knockout mice (KO mice) were used as the model for fragile X syndrome.The results of step-through and step-down tests demonstrated that Fmr1 KO mice had shorter latencies and more error counts,indicating a learning and memory disorder.After treatment with 30,60,90,120,or 200 mg/kg lithium chloride,the learning and memory abilities of the Fmr1 KO mice were significantly ameliorated,in particular,the 200 mg/kg lithium chloride treatment had the most significant effect.Western blot analysis showed that lithium chloride significantly enhanced the expression of phosphorylated glycogen synthase kinase 3 beta,an inactive form of glycogen synthase kinase 3 beta,in the cerebral cortex and hippocampus of the Fmr1 KO mice.These results indicated that lithium chloride improved learning and memory in the Fmr1 KO mice,possibly by inhibiting glycogen synthase kinase 3 beta activity. 展开更多
关键词 fragile X syndrome Fmr1 knockout mice step-down test step-through test learning and memory glycogen synthase kinase 3 beta lithium chloride
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Kongsheng Zhenzhong pill's effect on the learning and memory ability and its neuroprotective effects in vascular dementia rats 被引量:3
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作者 Xuming Ji Huayun Yu +4 位作者 Bin Ouyang Guowei Liu Zhichun Wu Heng Liu Fang Du 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2342-2346,共5页
Clinical reports have demonstrated that the Kongsheng Zhenzhong pill (KSZZP), a classical prescription deriving from Valuable Prescription for Emergencies, has good therapeutic effects on vascular dementia. However,... Clinical reports have demonstrated that the Kongsheng Zhenzhong pill (KSZZP), a classical prescription deriving from Valuable Prescription for Emergencies, has good therapeutic effects on vascular dementia. However, the mechanisms that mediate its effects remain unclear. In this study, the expression of N-methyI-D-aspartate receptor 1 mRNA, the content of nitric oxide, and the concentration of calcium in neurons was determined with in situ hybridization, spectrophotometry and flow cytometry, respectively. In addition, the expressions of N-methyI-D-aspartate receptor 1, nerve growth factor protein, and glial cell line-derived neurotrophic factor protein were detected with immunohistochemistry. We found that KSZZP could significantly decrease the expression of N-methyI-D-aspartate receptor 1 mRNA and protein, the content of nitric oxide, and the concentration of calcium in neurons. KSZZP also increased the expression of nerve growth factor and glial cell line-derived neurotrophic factor protein in the hippocampus CA1 region and in the cerebral cortex. Morris water maze and passive avoidance tests verified that KSZZP ameliorated the cognitive impairments of vascular dementia rats. Moreover, the KSZZP-induced improvements in the cognitive functions of vascular dementia rats were correlated with both inhibition of N-methyl-D-aspartate-induced excitable neurotoxicity and elevation of neurotrophic factor expression. 展开更多
关键词 Kongsheng Zhenzhong pill vascular dementia learning and memory ability neuroprotective effects
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Protective Effect of Ginkgo Biloba Leaf Extract on Learning and Memory Deficit Induced by Aluminum in Model Rats 被引量:4
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作者 龚其海 吴芹 +3 位作者 黄燮南 孙安盛 聂晶 石京山 《Chinese Journal of Integrated Traditional and Western Medicine》 2006年第1期37-41,共5页
Objective: To examine the protective effect of Ginkgo biloba leaf extract (GbE) on learning and memory deficit induced by aluminum chloride (AlCl3), and explore its mechanisms. Methods: The rat models with learn... Objective: To examine the protective effect of Ginkgo biloba leaf extract (GbE) on learning and memory deficit induced by aluminum chloride (AlCl3), and explore its mechanisms. Methods: The rat models with learning and memory deficit were induced by administering via gastrogavage and drinking of AlCl3 solution. And the model rats were treated with GbE at the dose of 50, 100, 200 mg/kg every day for 2 months accompanied with drinking of AlCl3 solution, respectively. Their abilities of spatial learning and memory were tested by Morris water maze, and the acetylcholinesterase (ACHE) activity in serum was assayed with chemical method, the AChE expression in hippocampus was observed by immunohistochemistry assay, and then quantitative analysis was done by BI 2000 image analysis system. Results: Learning and memory deficit of rats could be induced by AlCl3 solution (P〈0.01), and AChE expressions in rats hippocampus were increased (P〈0.01); GbE ameliorated learning and memory deficit and reduced AChE expression in rats hippocampus in a dose-dependent manner, while GbE significantly increased serum AChE activity at the dose of 200 mg/kg each day (P〈0.05). Conclusion: GbE can ameliorate learning and memory deficit induced by AlCl3, which may be due to its inhibition of the AChE expression in hippocampus. 展开更多
关键词 Ginkgo biloba leaf extract aluminum chloride learning and memory ACETYLCHOLINESTERASE RATS
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Similar effects of substance P on learning and memory function between hippocampus and striatal marginal division 被引量:2
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作者 Yan Yu Changchun Zeng +2 位作者 Siyun Shu Xuemei Liu Chuhua Li 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第8期857-863,共7页
Substance P is an endogenous neurokinin that is present in the central and peripheral nervous systems. The neuropeptide substance P and its high-affinity receptor neurokinin 1 receptor are known to play an important r... Substance P is an endogenous neurokinin that is present in the central and peripheral nervous systems. The neuropeptide substance P and its high-affinity receptor neurokinin 1 receptor are known to play an important role in the central nervous system in inflammation, blood pressure, motor behavior and anxiety. The effects of substance P in the hippocampus and the marginal di- vision of the striatum on memory remain poorly understood. Compared with the hippocampus as a control, immunofluorescence showed high expression of the substance P receptor, neuro- kinin 1, in the marginal division of the striatum of normal rats. Unilateral or bilateral injection of an antisense oligonucleotide against neurokinin 1 receptor mRNA in the rat hippocampus or marginal division of the striatum effectively reduced neurokinin 1 receptor expression. Indepen- dent of injection site, rats that received this antisense oligonucleotide showed obviously increased footshock times in a Y-maze test. These results indicate that the marginal division of the striatum plays a similar function in learning and memory to the hippocampus, which is a valuable addi- tion to our mechanistic understanding of the learning and memory functions of the marginal division of the striatum. 展开更多
关键词 nerve regeneration cognition substance P neurokinin 1 receptor HIPPOCAMPUS margin-al division of the striatum learning and memory NEOSTRIATUM NSFC grant neural generation
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Wendan decoction improves learning and memory deficits in a rat model of schizophrenia 被引量:2
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作者 Cuiping Yang Changchun Cai +5 位作者 Xiaojin Yang Yanping Yang Zhigang Zhou Jianhua Liu Heping Ye HongjiaoWan 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第15期1132-1137,共6页
An experimental model of schizophrenia was established using dizocilpine (MK-801). Rats were intragastrically administered with Wendan decoction or clozapine for 21 days prior to establishing the model. The results ... An experimental model of schizophrenia was established using dizocilpine (MK-801). Rats were intragastrically administered with Wendan decoction or clozapine for 21 days prior to establishing the model. The results revealed that the latency of schizophrenia model rats to escape from the hidden platform in the Morris water maze was significantly shortened after administration of Wendan decoction or clozapine. In addition, the treated rats crossed the platform significantly more times than the untreated model rats. Moreover, the rate of successful long-term potentiation induction in the Wendan decoction group and clozapine group were also obviously increased compared with the model group, and the population spike peak latency was significantly shortened. These experimental findings suggest that Wendan decoction can improve the learning and memory ability of schizophrenic rats to the same extent as clozapine treatment. 展开更多
关键词 Wendan decoction SCHIZOPHRENIA Morris water maze long-term potentiation HIPPOCAMPUS learning and memory traditional Chinese medicine neural regeneration
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Protective effect of tetrahydroxy stilbene glucoside on learning and memory by regulating synaptic plasticity 被引量:2
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作者 Hong-bo Luo Yun Li +6 位作者 Zun-jing Liu Li Cao Zhi-qiang Zhang Yong Wang Xiao-yan Zhang Zhao Liu Xiang-qun Shi 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第9期1480-1486,共7页
Damage to synaptic plasticity induced by neurotoxicity of amyloid-beta is regarded to be one of the pathological mechanisms of learning and memory disabilities in Alzheimer's disease patients. This study assumed that... Damage to synaptic plasticity induced by neurotoxicity of amyloid-beta is regarded to be one of the pathological mechanisms of learning and memory disabilities in Alzheimer's disease patients. This study assumed that the damage of amyloid-beta to learning and memory abilities was strongly associated with the changes in the Fyn/N-methyl-D-aspartate receptor 2B (NR2B) expression. An APP695V7171 transgenic mouse model of Alzheimer's disease was used and treatment with tetrahydroxy-stilbene glucoside was administered intragas- trically. Results showed that intragastric administration of tetrahydroxy-stilbene glucoside improved the learning and memory abilities of the transgenic mice through increasing NR2B receptors and Fyn expression. It also reversed parameters for synaptic interface structure of gray type I. These findings indicate that tetrahydroxy stilbene glucoside has protective effects on the brain, and has prospects for its clinical application to improve the learning and memory abilities and treat Alzheimer's disease. 展开更多
关键词 nerve regeneration tetrahydroxy stilbene glucoside AIzheimer's disease AMYLOID-BETA cognitive impairment learning and memory synaptic plasticity Fyn/N-methyl-D-aspartate receptor 2B signaling pathway NEUROPROTECTION neural regeneration
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Ganoderma lucidum spore powder modulates Bcl-2 and Bax expression in the hippocampus and cerebral cortex,and improves learning and memory in pentylenetetrazole-kindled rats 被引量:2
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作者 Shuang Zhao Shengchang Zhang Shuqiu Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2347-2351,共5页
We studied the effects of Ganoderma lucidum spore powder on Bax and Bcl-2 expression and neuronal apoptosis in pentylenetetrazole-kindled epileptic rats. Sixty adult rats were randomly divided into a control group, an... We studied the effects of Ganoderma lucidum spore powder on Bax and Bcl-2 expression and neuronal apoptosis in pentylenetetrazole-kindled epileptic rats. Sixty adult rats were randomly divided into a control group, an epileptic group (kindled) and three medication groups (150,300 450 mg/kg given to kindled rats). Bax and Bcl-2 immunohistochemistry and TUNEL labeling showed that the number of Bax- and TUNEL-positive cells in the hippocampus and cerebral cortex decreased significantly in the high-dose medication group, while the number of Bcl-2 immunoreactive cells increased. The Morris water maze test showed that high-dose treatment significantly shortened escape latency and increased spatial probe trial performance. Our findings indicate that a high dose of Ganoderma lucidum spore powder upregulates the expression of antiapoptotic Bcl-2 protein in the hippocampus and cerebral cortex, inhibits proapoptotic Bax expression, and decreases seizure-induced neuronal apoptosis. Further, Ganoderma lucidum appears to protect against epilepsy-related learning and memory impairments. 展开更多
关键词 Ganoderma lucidum spore powder EPILEPSY BAX BCL-2 learning and memory neural regeneration
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The Screening of Genes Sensitive to Long-Term, Low-Level Microwave Exposure and Bioinformatic Analysis of Potential Correlations to Learning and Memory 被引量:2
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作者 ZHAO Ya Li LI Ying Xian +6 位作者 MA Hong Bo LI Dong LI Hai Liang JIANG Rui KAN Guang Han YANG Zhen Zhong HUANG Zeng Xin 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2015年第8期558-570,共13页
Objective To gain a better understanding of gene expression changes in the brain following microwave exposure in mice. This study hopes to reveal mechanisms contributing to microwave-induced learning and memory dysfun... Objective To gain a better understanding of gene expression changes in the brain following microwave exposure in mice. This study hopes to reveal mechanisms contributing to microwave-induced learning and memory dysfunction. Methods Mice were exposed to whole body 2100 MHz microwaves with specific absorption rates (SARs) of 0.45 W/kg, 1.8 W/kg, and 3.6 W/kg for 1 hour daily for 8 weeks. Differentially expressing genes in the brains were screened using high-density oligonucleotide arrays, with genes showing more significant differences further confirmed by RT-PCR. Results The gene chip results demonstrated that 41 genes (0.45 W/kg group), 29 genes (1.8 W/kg group), and 219 genes (3.6 W/kg group) were differentially expressed. GO analysis revealed that these differentially expressed genes were primarily involved in metabolic processes, cellular metabolic processes, regulation of biological processes, macromolecular metabolic processes, biosynthetic processes, cellular protein metabolic processes, transport, developmental processes, cellular component organization, etc. KEGG pathway analysis showed that these genes are mainly involved in pathways related to ribosome, Alzheimer's disease, Parkinson's disease, long-term potentiation, Huntington's disease, and Neurotrophin signaling. Construction of a protein interaction network identified several important regulatory genes including synbindin (sbdn), Crystallin (CryaB), PPP1CA, Ywhaq, Psap, Psmb1, Pcbp2, etc., which play important roles in the processes of learning and memory. Conclusion Long-term, low-level microwave exposure may inhibit learning and memory by affecting protein and energy metabolic processes and signaling pathways relating to neurological functions or diseases. 展开更多
关键词 LONG-TERM Low-level MICROWAVE Gene chip learning and memory
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