期刊文献+
共找到152篇文章
< 1 2 8 >
每页显示 20 50 100
Long-term potentiation-based screening identifies neuronal PYGM as a synaptic plasticity regulator participating in Alzheimer's disease 被引量:3
1
作者 Ting Wang Yun-Qiang Zhou +11 位作者 Yong Wang Liang Zhang Xiang Zhu Xiu-Yan Wang Jing-Hui Wang Lin-Kun Han Jian Meng Xian Zhang Hong Luo Qi-Lin Ma Zhan-Xiang Wang Yun-Wu Zhang 《Zoological Research》 SCIE CSCD 2023年第5期867-881,共15页
Synaptic dysfunction is an important pathological hallmark and cause of Alzheimer's disease(AD).High-frequency stimulation(HFS)-induced long-term potentiation(LTP)has been widely used to study synaptic plasticity,... Synaptic dysfunction is an important pathological hallmark and cause of Alzheimer's disease(AD).High-frequency stimulation(HFS)-induced long-term potentiation(LTP)has been widely used to study synaptic plasticity,with impaired LTP found to be associated with AD.However,the exact molecular mechanism underlying synaptic plasticity has yet to be completely elucidated.Whether genes regulating synaptic plasticity are altered in AD and contribute to disease onset also remains unclear.Herein,we induced LTP in the hippocampal CA1 region of wildtype(WT)and AD model mice by administering HFS to the CA3 region and then studied transcriptome changes in the CA1 region.We identified 89 genes that may participate in normal synaptic plasticity by screening HFS-induced differentially expressed genes(DEGs)in mice with normal LTP,and 43 genes that may contribute to synaptic dysfunction in AD by comparing HFS-induced DEGs in mice with normal LTP and AD mice with impaired LTP.We further refined the 43 genes down to 14 by screening for genes with altered expression in pathological-stage AD mice without HFS induction.Among them,we found that the expression of Pygm,which catabolizes glycogen,was also decreased in AD patients.We further demonstrated that down-regulation of PYGM in neurons impaired synaptic plasticity and cognition in WT mice,while its overexpression attenuated synaptic dysfunction and cognitive deficits in AD mice.Moreover,we showed that PYGM directly regulated energy generation in neurons.Our study not only indicates that PYGM-mediated energy production in neurons plays an important role in synaptic function,but also provides a novel LTP-based strategy to systematically identify genes regulating synaptic plasticity under physiological and pathological conditions. 展开更多
关键词 Alzheimer's disease High-frequency stimulation long-term potentiation PYGM Synaptic plasticity TRANSCRIPTOME
下载PDF
Effects of the ephedra alkaloid methylephedrine on the basal evoked potential transportation and the long-term potentiation (LTP) in the rat hippocampal dentate granule cells in vivo
2
作者 PENG Xiao-dong(Department of Pharmacology,Ningxia Medical University,Yinchuan 750004,China) 《沈阳药科大学学报》 CAS CSCD 北大核心 2008年第S1期62-62,共1页
Objective The effect of the ephedra/ephedrine alkaloid methylephedrine(dl-methylephedrine hydrochloride for testing in this paper)on cognitive related synaptic plasticity was investigated by recording extracellular fi... Objective The effect of the ephedra/ephedrine alkaloid methylephedrine(dl-methylephedrine hydrochloride for testing in this paper)on cognitive related synaptic plasticity was investigated by recording extracellular field evoked potentials and its LTP in hippocampal dentate granule cells in urethane-anaesthetized rats in vivo.Methods Single pathway recording of evoked field potentials was made from the dentate granule cells of hippocampal hemisphere in response to stimulation of the ipsilateral medial perforant path(MPP).Two parameters,the amplitude of population spike(PS amplitude)and the latency of the PS,were employed to evaluate the effects of drug on the overall changes in cellular responses.Results The present study show that methylephedrine 90 mg·kg-1 intraperitoneally,about 1/3 LD50,could increase the latency of the PS in hippocampal dentate granule cells by constant single stimulation of the MPP as the basal ransportation.However,the 30 mg·kg-1 and 10 mg·kg-1 dosage had no effect on the latency,and there are no influences of PS amplitude for all examinational groups.The methylephedrine 90 mg·kg-1 group significant enhanced the development of amplitude LTP in hippocampal dentate granule cells that induced by 60 Hz,60 pulses conditional tetanus in medial perforant path area.Also,the 30 mg·kg-1 group can promoted the maintenance of LTP induced by this tetanus,but no promotion on PS amplitude LTP appeared in this dosage and no any changes been found in 10 mg·kg-1 dosage group.Conclusions The ephedra/ephedrine alkaloid methylephedrine can modulate the synaptic plasticity in the lateral perforant path.A possible mechanism of methylephedrine on hippocampal LTP is been discussed. 展开更多
关键词 EPHEDRA methylephedrine EVOKED potential ltp HIPPOCAMPAL GRANULE cells in vivo
下载PDF
Aniracetam attenuates H_2O_2-induced deficiency of neuron viability, mi-tochondria potential and hippocampal long-term potentiation of mice in vitro 被引量:1
3
作者 王永富 李朝翠 蔡景霞 《Neuroscience Bulletin》 SCIE CAS CSCD 2006年第5期274-280,共7页
Objective It is known that free radicals are involved in neurodegeneration and cognitive dysfunction, as seen in Alzheimer's disease (AD) and aging. The present study examines the protective effects of aniracetam a... Objective It is known that free radicals are involved in neurodegeneration and cognitive dysfunction, as seen in Alzheimer's disease (AD) and aging. The present study examines the protective effects of aniracetam against H2O2- induced toxicity to neuron viability, mitochondria potential and hippocampal long-term potentiation (LTP). Methods Tetrazolium salt 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) was used to detect neuronal viability. MitoTracker Red (CMX Ros), a fluorescent stain for mitochondria, was used to measure mitochondria potential. Electrophysiological technique was carried out to record hippocampual LTE Results H2O2 exposure impaired the viability of neurons, reduced mitochondria potential, and decreased LTP in the CA region of hippocampus. These deficient effects were significantly rescued by pre-treatment with aniracetam (10 ~100μmol/L). Conclusion These results indicate that aniracetam has a strong neuroprotective effect against H2O2-induced toxicity, which could partly explain the mechanism of its clinical application in neurodegenerative diseases. 展开更多
关键词 H2O2 ANIRACETAM neuronal viability mitochondria potential long-term potentiation hippocampus MICE
下载PDF
Effects of Chronic Administration of Melatonin on Spatial Learning Ability and Long-term Potentiation in Lead-exposed and Control Rats 被引量:4
4
作者 XIU-JING CAO MING WANG +3 位作者 WEI-HENG CHEN DA-MIAO ZHU JIA-QI SHE DI-YUN RUAN 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2009年第1期70-75,共6页
Objective To explore the changes in spatial learning performance and long-term potentiation (LTP) which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after... Objective To explore the changes in spatial learning performance and long-term potentiation (LTP) which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after administration of melatonin (MT) for two months. Methods Experiment was performed in adult male Wistar rats (12 controls, 12 exposed to melatonin treatment, 10 exposed to lead and 10 exposed to lead and melatonin treatment). The lead-exposed rats received 0.2% lead acetate solution from their birth day while the control rats drank tap water. Melatonin (3 mg/kg) or vehicle was administered to the control and lead-exposed rats from the time of their weaning by gastric gavage each day for 60 days, depending on their groups. At the age of 81-90 days, all the animals were subjected to Morris water maze test and then used for extracellular recording of LTP in the dentate gyrus (DG) area of the hippocampus in vivo. Results Low dose of melatonin given from weaning for two months impaired LTP in the DG area of hippocampus and induced learning and memory deficit in the control rats. When melatonin was administered over a prolonged period to the lead-exposed rats, it exacerbated LTP impairment, learning and memory deficit induced by lead. Conclusion Melatonin is not suitable for normal and lead-exposed children. 展开更多
关键词 MELATONIN LEAD Learning MEMORY long-term potentiation (ltp
下载PDF
Effects of Exposure to Aluminum on Long-term Potentiation and AMPA Receptor Subunits in Rats in vivo 被引量:14
5
作者 SONG Jing LIU Ying +2 位作者 ZHANG Hui Fang ZHANG Qin Li NIU Qiao 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2014年第2期77-84,共8页
Objective To explore the effects of exposure to aluminum (AI) on long-term potentiation (LTP) and AMPA receptor subunits in rats in vivo. Methods Different dosages of aluminum-maltolate complex [Al(mal)3] were g... Objective To explore the effects of exposure to aluminum (AI) on long-term potentiation (LTP) and AMPA receptor subunits in rats in vivo. Methods Different dosages of aluminum-maltolate complex [Al(mal)3] were given to rats via acute intracerebroventricular (i.c.v.) injection and subchronic intraperitoneal (i.p.) injection. Following AI exposure, the hippocampal LTP were recorded by field potentiation technique in vivo and the expression of AMPAR subunit proteins (GluR1 and GluR2) in both total and membrane-enriched extracts from the CA1 area of rat hippocampus were detected by Western blot assay. Results Acute AI treatment produced dose-dependent suppression of LTP in the rat hippocampus and dose-dependent decreases of GluRz and GluR2 in membrane extracts; however, no similar changes were found in the total cell extracts, which suggests decreased trafficking of AMPA receptor subunits from intracellular pools to synaptic sites in the hippocampus. The dose-dependent suppressive effects on LTP and the expression of AMPA receptor subunits both in the membrane and in total extracts were found after subchronic AI treatment, indicating a decrease in AMPA receptor subunit trafficking from intracellular pools to synaptic sites and an additional reduction in the expression of the subunits. Conclusion Al(mal)3 obviously and dose-dependently suppressed LTP in the rat hippocampal CA1 region in vivo, and this suppression may be related to both trafficking and decreases in the expression of AMPA receptor subunit proteins. However, the mechanisms underlying these observations need further investigation. 展开更多
关键词 Aluminum-maltolate complex long-term potentiation AMPA receptor HIPPOCAMPUS INVIVO
下载PDF
The RAS/PI3K Pathway is Involved in the Impairment of Long-term Potentiation Induced by Acute Aluminum Treatment in Rats 被引量:6
6
作者 SONG Jing LIU Ying +1 位作者 ZHANG Hui Fang NIU Qiao 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2016年第11期782-789,共8页
Objective To explore the role of RAS/PI3K pathway in the impairment of long-term potentiation (LTP) induced by acute aluminum (AI) treatment in rats in vivo. Methods First, different dosages of aluminum-maltolate ... Objective To explore the role of RAS/PI3K pathway in the impairment of long-term potentiation (LTP) induced by acute aluminum (AI) treatment in rats in vivo. Methods First, different dosages of aluminum-maltolate complex [Al(mal)3] were given to rats via acute intracerebroventricular (i.c.v.) injection. Following AI exposure, the RAS activity of rat hippocampus were detected by ELISA assay after the hippocampal LTP recording by field potentiation technique in vivo. Second, the antagonism on the aluminum-induced suppression of hippocampal LTP was observed after the treatment of the RAS activator epidermal growth factor (EGF). Finally, the antagonism on the downstream molecules (PKB activity and the phosphorylation of GluR1 $831 and $845) were tested by ELISA and West-blot assays at the same time. Results With the increasing aluminum dosage, a gradually decreasing in RAS activity of the rat hippocampus was produced after a gradually suppressing on LTP. The aluminum-induced early suppression of hippocampal LTP was antagonized by the RAS activator epidermal growth factor (EGF). And the EGF treatment produced changes similar to those observed for LTP between the groups on PKB activity as well as the phosphorylation of GluR1 S831 and s845. Conclusion The RAS-PI3K/PKB-GluR1 S831 and S845 signal transduction pathway may be involved in the inhibition of hippocampal LTP by aluminum exposure in rats. However, the mechanisms underlying this observation need further investigation. 展开更多
关键词 ALUMINUM long-term potentiation RAS PKB AMPA receptor
下载PDF
Active fraction combination from Liuwei Dihuang decoction(LW-AFC) ameliorates corticosterone-induced long-term potentiation impairment in mice in vivo 被引量:4
7
作者 HUANG Yan LI Dong +3 位作者 CHENG Bin LIU Gang ZHANG Yong-xiang ZHOU Wen-xia 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第6期436-437,共2页
Liuwei Dihuang decoction(LW), a classic formula in traditional Chinese medicine(TCM), has been used for nearly one thousand years for various diseases with characteristic features of kidney yin deficiency. LW consists... Liuwei Dihuang decoction(LW), a classic formula in traditional Chinese medicine(TCM), has been used for nearly one thousand years for various diseases with characteristic features of kidney yin deficiency. LW consists of 6herbs including Dihuang[prepared root of Rehmannia glutinosa(Gaertn) DC], Shanyao(rhizome of Dioscorea polystachya Turcz), Shanzhuyu(fruit of Cornus officinalis Siebold Zucc), Mudanpi(root bark of Paeonia × suffruticosa Andrews),Zexie(rhizome of Alisma plantago-aquatica L) and Fuling(scleorotia of Wolfiporia extensa(Peck) Ginns)LW-active fraction combination(LW-AFC) is extracted from LW, it is effective for the treatment of kidney yin deficiency in many animal models. There are 3 fractions in LW-AFC, a polysaccharide fraction(LWB-B), a glycoside fraction(LWD-b) and an oligosaccharide fraction(CA-30). Our previous results indicate that LW-AFC has similar pharmacological effects to LW, modulating the balance of the NIM network. LW-AFC has positive effects in many animal models of kidney deficiency or disturbance of the NIM network. LW-AFC could improve the cognitive ability in Alzheimer′s disease(AD) animal models(APP/PS1, SAMP8), where modulating immune function and balancing the NIM network may play an important role in its cognition improving effects. Our study also showed that LW-AFC had protective effects on stress-induced disturbances of the NIM network. However, the underlying mechanisms remain elusive and need further investigation. OBJECTIVE This study evaluated the effects of LW-AFC and the active fractions(polysaccharide, LWB-B;glycoside, LWD-b;oligosaccharide,CA-30) on corticosterone(Cort)-induced long-term potentiation(LTP) impairment in vivo. METHODS LTP was used to evaluate the synaptic plasticity. LW-AFC was orally administered for seven days. The active fractions were given by either chronic administration(ig, ip, 7 d) or single administration(icv, ig, ip). Cort was injected subcutaneously 1 h before the high-frequency stimulation(HFS) to induce LTP impairment. Moreover, in order to research on the possible effective pathways, an antibiotic cocktail and an immunosuppressant were also used. RESULTS Chronic administration(ig) of LW-AFC and its three active fractions could ameliorate Cort-induced LTP impairment. Single administration(icv, ig, ip) of any of the active fractions had no effect on Cort-induced LTP impairment, while chronic administration(ig, ip) of LWB-B or LWD-b showed positive effects against Cort. Interestingly, CA-30 only showed protective effects via ig administration,and there was little effect when CA-30 was administered ip In addition, when the intestinal microbiota was disrupted by application of the antibiotic cocktail, CA-30 showed little protective effects against Cort. The effects of LW-AFC were also abolished when the immune function was inhibited. In the hippocampal tissue, Cort treatment increased corticosterone and glutamate, and LW-AFC could inhibit the Cort-induced elevation of corticosterone and glutamate;there was little change in D-serine in Cort-treated animals, but LW-AFC could increase the D-serine levels. CONCLUSION LW-AFC and its three active fractions could ameliorate Cort-induced LTP impairment. Their protective effects are unlikely by a direct way, and immune modulation might be the common pathway. CA-30 could protect LTP from impairment via modulating the intestinal microbiota. Decreasing corticosterone and glutamate and increasing D-serine in the Cort-treated animals’ hippocampal tissue might be one of the mechanisms for the neural protective effects of LW-AFC. Further study is needed to understand the underlying mechanisms. 展开更多
关键词 LW-active fraction COMBINATION ACTIVE FRACTIONS CORTICOSTERONE long-term potentiation SYNAPTIC plasticity stress
下载PDF
Electric stimulation at sciatic nerve evokes long-term potentiation of cornu dorsale medullae spinalis field potential in rats at various developmental phases 被引量:1
8
作者 Jiang Wu Dan Shu Qisheng Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2007年第7期385-389,共5页
BACKGROUND: Long-term potentiation of cornu dorsale medullae spinalis field potential in adult rats has already been reported; however, there is lack of correlated researches on naenonate, infant and adult rats which... BACKGROUND: Long-term potentiation of cornu dorsale medullae spinalis field potential in adult rats has already been reported; however, there is lack of correlated researches on naenonate, infant and adult rats which have different responses to pain conduction information.OBJECTIVE: To observe the various effects of electric stimulation at sciatic nerve on long-term potentiation of evoked field potential at superficial layer of cornu dorsale medullae spinalis of rats at various developmental phases and analyze manifestations of pain conduction information at superficial layers ( Ⅰ - Ⅱ)of cornu dorsale medullae spinalis in immature rats.DESIGN: Grouping controlled study.SETTING: Department of Physiology, Medical College of Wuhan University.MATERIALS: The experiment was carried out in the Laboratory of Physiology (provincial laboratory),Medical College of Wuhan University from March 2006 to May 2007. A total of 27 healthy male Sprague-Dawley (SD) rats, 17- 90 days old, SPF grade, weighing 41 -200 g, were provided by Experimental Animal Center, Medical College of Wuhan University.METHODS: Based on their birthdays, rats were divided into naenonate group (17 - 20 days old, weighing 41-52 g, n =10), infant group (35 - 50 days old, weighing 87 - 125 g, n =10) and adult group (60 - 90 days old, weighing 180 -200 g, n =7). Left sciatic nerve was separated and stimulated with single square wave (15 V, 0.5 ms). Meanwhile, evoked field potential was recorded at superficial layers of lateral T13 - L1 cornu dorsale medullae spinalis and then stimulated with high-frequent and high-intensive tetanizing current (30 -40 V, 0.5 ms, 100 Hz, 1s per bundle, 10s in bundle interval) four times. After the operation, onset of long-term potentiation was observed; meanwhile, amplitude changes and latency of field potential were analyzed.MAIN OUTCOME MEASURES: Amplitude and latency changes of field potential at superficial layers of cornu dorsale medullae spinalis of rats in the three groups.RESULTS: A total of 27 accepted rats were involved in the final analysis. ① Amplitude changes: Electric stimulation at sciatic nerve with high-frequent and high-intensive tetanizing current could induce evoked field potential at superficial layers (Ⅰ-Ⅱ ) of cornu dorsale medullae spinalis in the three groups.Long-term potentiation in the naenonate group manifested that amplitude of A-kind never fiber was raised and there was significant difference (P〈0.05). In addition, average amplitude was increased and there was obviously significant difference (P〈0.01). Long-term potentiation in the infant group manifested that amplitude of C-kind never fiber was raised and there was significant difference (P〈0.01); while, long-term potentiation in the adult group manifested that amplitude of C-kind never fiber was raised and there was significant difference (P〈0.01). Otherwise, latencies in the three groups were all shortened. ② Latency changes: Average latency of A-kind nerve fiber in the naenonate group was shortened and there was significant difference (P〈0.01); in addition, evoked potential of C-kind nerve fiber was low and latency was immovable. There was no significant difference before and after high-frequent and high-intensive electric stimulation (P〉0.05). Average latency of C-kind nerve fiber in the infant group was shortened and there was significant difference (P〈0.01); in addition, evoked potential of A-kind nerve fiber was stable and latency was immovable. There was no significant difference before and after high-frequent and high-intensive electric stimulation (P〉0.05). Average latency of C-kind nerve fiber in the adult group was shortened and there was significant difference (P〈0.01); in addition, evoked potential of A-kind nerve fiber was stable and latency was immovable. There was no significant difference before and after high-frequent and high-intensive electric stimulation.CONCLUSION: Evoked field potential at superficial layer of comu dorsale medullae spinalis can be recorded through electric stimulation at sciatic nerve. Single stimulation and tetanizing electric stimulation can cause different characteristics of evoked field potential in rats at various developmental phases.Superficial layer of cornu dorsale medullae spinalis of naenonate rats is mainly caused by A-kind nerve fiber which participants in pain conduction and formation of pain sensitivity; however, that of infant and adult rats mainly depends on C-kind nerve fiber. 展开更多
关键词 long-term potentiation spinal cord electric stimulation
下载PDF
Effect of Aluminum on Long-Term Potentiation and Its Relation to L-arg-No-pathway in Hippocampal CA3 Area of Rats 被引量:1
9
作者 邹本德 张自东 +1 位作者 肖鸿美 李艾 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 1998年第4期193-196,200,共5页
Experiments were performed on 64 Sprague-Dawley rats under ure-thane anesthesia. Extracellular recording method was used to investigate the effect of aluminum (Al)microinjected into CA3 on long-term potentiation (LTP)... Experiments were performed on 64 Sprague-Dawley rats under ure-thane anesthesia. Extracellular recording method was used to investigate the effect of aluminum (Al)microinjected into CA3 on long-term potentiation (LTP) in this area. The relationship between the inhibitory effect of Al and L-arginine-NO pathway was also studied. Microinjection of Al (0. 5 mol/L, 1 μl ) into CA3 could block the induction of LTP in CA3. Microinjection of Al (0. 5 mol/L, 1 μl) into CA3 after LTP was induced could also decrease the amplitude of population spike (PS). The inhibitory effect of Al on LTP in CA3 could be enhanced by preinjection of NG-nitro-L-arginine (0. 3 mol/L, 1 μl). Preinjection of L-arginine (0. 3 mol/L, 1 μl) into CA3 could antagonize the inhibitory effect of Al on LTP. These results suggest that Al could block the induction of LTP and decrease the amplitude of PS potentiated in CA3. The effect of Al might be antagonized by L-arginine-NO pathway. 展开更多
关键词 CA3 area of hippocampus long-term potentiation ALUMINUM NG-ni-tro-L-arginine L-ARGININE
下载PDF
Correlating learning and memory improvements to long-term potentiation in patients with brain injury
10
作者 Xingfu Peng Qian Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第2期172-176,共5页
BACKGROUND: Brain injury patients often exhibit learning and memory functional deficits. Long-term potentiation (LTP) is a representative index for studying learning and memory cellular models; the LTP index correl... BACKGROUND: Brain injury patients often exhibit learning and memory functional deficits. Long-term potentiation (LTP) is a representative index for studying learning and memory cellular models; the LTP index correlates to neural plasticity. OBJECTIVE: This study was designed to investigate correlations of learning and memory functions to LTP in brain injury patients, and to summarize the research advancements in mechanisms underlying brain functional improvements after rehabilitation intervention. RETRIEVAL STRATEGY: Using the terms "brain injuries, rehabilitation, learning and memory, long-term potentiation", manuscripts that were published from 2000-2007 were retrieved from the PubMed database. At the same time, manuscripts published from 2000-2007 were also retrieved from the Database of Chinese Scientific and Technical Periodicals with the same terms in the Chinese language. A total of 64 manuscripts were obtained and primarily screened. Inclusion criteria: studies on learning and memory, as well as LTP in brain injury patients, and studies focused on the effects of rehabilitation intervention on the two indices; studies that were recently published or in high-impact journals. Exclusion criteria: repetitive studies. LITERATURE EVALUATION: The included manuscripts primarily focused on correlations between learning and memory and LTP, the effects of brain injury on learning and memory, as well as LTP, and the effects of rehabilitation intervention on learning and memory after brain injury. The included 39 manuscripts were clinical, basic experimental, or review studies. DATA SYNTHESIS: Learning and memory closely correlates to LTP. The neurobiological basis of learning and memory is central nervous system plasticity, which involves neural networks, neural circuits, and synaptic connections, in particular, synaptic plasticity. LTP is considered to be an ideal model for studying synaptic plasticity, and it is also a classic model for studying neural plasticity of learning and memory. Brain injury patients clinically present with various manifestations, such as paralysis and sensory disability, which closely correlate to injured regions. In addition, learning and memory abilities decrease in brain injury patients and LTP decreases following brain injury. Brain tissue injury will lead to brain functional deficits. Hippocampal LTP is very sensitive. Difficulties in LTP induction are apparent even prior to morphological changes in brain tissue. There are no specific treatments for learning and memory functional deficits following brain injury. At present, behavioral and compensative therapies are the typical forms of rehabilitation. These results indicate that rehabilitation promotes learning and memory functional recovery in brain injury patients by speeding up LTP formation in the hippocampal CA3 region. CONCLUSION: Rehabilitation intervention increases LTP formation in the hippocampal CA3 region and recovers learning and memory functions in brain injury patients. 展开更多
关键词 learning and memory brain injury long-term potentiation REHABILITATION
下载PDF
LW-AFC and its active components ameliorate corticosterone-induced long-term potentiation impairment in mice
11
作者 Yan HUANG Dong LI +1 位作者 Wen-xia ZHOU Yong-xiang ZHANG 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2017年第10期989-990,共2页
OBJECTIVE LW-AFC is extracted from the classical traditional Chinese medicinal prescription-Liuwei Dihuang Decoction.Previous studies have showed that LW-AFC could improve learning&memory ability in amny animal mo... OBJECTIVE LW-AFC is extracted from the classical traditional Chinese medicinal prescription-Liuwei Dihuang Decoction.Previous studies have showed that LW-AFC could improve learning&memory ability in amny animal models.In this study,we focused on evaluating the effect of several main active components fromLW-AFC(B-B;loganin,LOG;morroniside,MOR;paeoniflorin,PF and stachyose,STA)on LTP.METHODS In vivo recording of LTP was used in this study to evaluate the effects of LW-AFC and it′s active components on coticorsterone(Cort)induced LTP impairment.RESULTS The results showed that LW-AFC could ameliorate Cort-induced LTP impairment.The effect of LW-AFC was abolished when the immune function was inhibited.Single administration(ig,ip,icv)of any of the components had no effect on Cort-induced LTP impairment.Consecutively intragastric administration or intraperitoneal injections(chronic administration)of B-B,LOG,MOR or PF for 7 d showed protective effect on Cort-induced LTP impairment.Intragastric administration of STA for 7 d protected LTP from impairment induced by Cort,while there was little improving effect when STA was administrated via intraperitoneal injection.In addition,when the intestinal microbiota was disrupted by applying the antibiotic cocktail,STA showed little protective effect against Cort.CONCLUSION In conclusion,LW-AFC and it′s components showed positive effects against cort induced LTP impairment,it seems that all displayed protective effects via indirectly,immune modulation might be the common pathway for all components;the exact pathways are different in each component,B-B,LOG,MOR and PF could be absorbed into the bloods tream and then modulate the peripheral immune function,while STA could not be absorbed and modulates the immune function via modulating intestinal microbiota.Further studies are needed to invesgate the underlying mechanisms and the synergetic effects of all components. 展开更多
关键词 LW-AFC active components synaptic plasticity long-term potentiation intestinal microbiota
下载PDF
Effects of electroacupuncture versus nimodipine on long-term potentiation and synaptophysin expression in a rat model of vascular dementia
12
作者 Dengming Wei Xuemin Jia Xiangxu Yin Wenwen Jiang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2357-2361,共5页
The present study stimulated Baihui (DU 20) and Dazhui (DU 14) acupoints in a rat model of vascular dementia with electroacupuncture to investigate changes in long-term potentiation and synaptophysin expression in... The present study stimulated Baihui (DU 20) and Dazhui (DU 14) acupoints in a rat model of vascular dementia with electroacupuncture to investigate changes in long-term potentiation and synaptophysin expression in the hippocampus. The results revealed that synaptophysin expression in brain tissues was increased after electroacupuncture. After high4requency stimulation, the population spike latency was shortened and the excitatory postsynaptic potential slope and population spike amplitude were increased. In addition, cognitive function was enhanced, similar to the effects of intragastric perfusion of nimodipine. The results indicated that electroacupuncture at Baihui and Dazhui acupoints can improve learning and memory functions of a rat model of vascular dementia by promoting synaptophysin expression, enhancing hippocampal synaptic plasticity and accelerating synaptic transmission. 展开更多
关键词 vascular dementia ELECTROACUPUNCTURE learning and memory ability long-term potentiation SYNAPTOPHYSIN neural regeneration
下载PDF
Mechanisms of active fraction combination from Liuwei Dihuang Decoction(LW-AFC) on long-term potentiation impairment in vivo
13
作者 HUANG Yan LI Dong +3 位作者 CHENG Bin LIU Gang ZHANG Yong-xiang ZHOU Wen-xia 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第9期665-665,共1页
OBJECTIVE Liuwei Dihuang Decoction(LW)-active fraction combination(LW-AFC,consist of 3 fractions polysaccharide,LWB-B;glycoside,LWD-b;oligosaccharide,CA-30)is extracted from LW,it is effective for the treatment of kid... OBJECTIVE Liuwei Dihuang Decoction(LW)-active fraction combination(LW-AFC,consist of 3 fractions polysaccharide,LWB-B;glycoside,LWD-b;oligosaccharide,CA-30)is extracted from LW,it is effective for the treatment of kidney yin deficiency in many animal models.This study evaluated the effects and mechanisms of LW-AFC and the active fractions on corticosterone(Cort)-induced long-term potentiation(LTP)impairment in vivo.METHODS LTP was used to evaluate the synaptic plasticity.LW-AFC was orally administered for seven days.The active fractions were given by either chronic administration(ig,ip,7 d)or single administration(icv,ig,ip).Cort was injected subcutaneously 1h before the high-frequency stimulation(HFS)to induce LTP impairment.Moreover,in order to research on the possible effective pathways,an antibiotic cocktail and an immunosuppressant were also used.RESULTS Chronic administration(ig)of LW-AFC and its three active fractions could ameliorate Cort-induced LTP impairment.Single administration(icv,ig,ip)of any of the active fractions had no effect on Cort-induced LTP impairment,while chronic administration(ig,ip)of LWB-B or LWD-b showed positive effects against Cort.Interestingly,CA-30 only showed protective effects via ig administration,and there was little effect when CA-30 was administered ip In addition,when the intestinal microbiota was disrupted by application of the antibiotic cocktail,CA-30 showed little protective effects against Cort.The effects of LW-AFC were also abolished when the immune function was inhibited.In the hippocampal tissue,Cort treatment increased Cort and glutamate,and LW-AFC could inhibit the Cort-induced elevation of Cort and glutamate;there was little change in D-serine in Cort-treated animals,but LW-AFC could increase the D-serine levels.CONCLUSION LW-AFC and its three active fractions could ameliorate Cort-induced LTP impairment.Their protective effects are unlikely by a direct way,and immune modulation might be the common pathway.CA-30 could protect LTP from impairment via modulating the intestinal microbiota.Decreasing Cort and glutamate and increasing D-serine in the Cort-treated animals'hippocampal tissue might be one of the mechanisms for the neural protective effects of LW-AFC.Further study is needed to understand the underlying mechanisms. 展开更多
关键词 LW-active fraction combination active fractions CORTICOSTERONE long-term potentiation synaptic plasticity stress
下载PDF
Corticosterone induced D-serine release deficit play an important role in long-term potentiation impairment by corticosterone in perforant path-dentate gyrus pathway
14
作者 HUANG Yan WANG Chen +4 位作者 YU Qi LI Dong SUN Na ZHANG Yong-xiang ZHOU Wen-xia 《中国药理学与毒理学杂志》 CAS 北大核心 2021年第10期764-764,共1页
OBJECTIVE Previous studies showed that over activation of NMDA receptors may be a crucial cause of long-term potentiation(LTP)and cognitive impairment induced by stress or corticosterone.However,other studies showed t... OBJECTIVE Previous studies showed that over activation of NMDA receptors may be a crucial cause of long-term potentiation(LTP)and cognitive impairment induced by stress or corticosterone.However,other studies showed that the function of NMDA receptors is insufficient since the NMDA receptors co-agonist D-serine could improve stress-induced cognitive impairment.The purpose of this study is to clarify whether over activation of NMDA receptors or hypofunction of NMDA receptors is involved in hippocampal impairment of LTP by corticosterone and the underlying mechanisms.METHODS Cort was injected subcutaneously 1 h before the high-frequency stimulation(HFS)to induce LTP impairment.NMDA receptor antagonists and agonists were administrated by icv.RESULTS Hippocampal LTP and object location recognition memory were impaired in corticosterone-treated mice.Corticosterone increased the glutamate level in hippocampal tissues,neither NMDA receptors antagonist nor its subtype antagonists alleviated impairment of LTP,while enhancing the function of NMDA receptors by D-serine did alleviate impairment of LTP by corticosterone,suggesting that hypofunction of NMDA receptors might be one of the main reasons for impairment of LTP by corticosterone.Further results showed that the level of D-serine and its precursor L-serine did not change.D-serine release-related protein Na+-independent alanine-serine-cysteine transporter-1(ASC-1)in the cell membrane was decreased and increasing D-serine release by the selective activator of ASC-1 antiporter activity alleviated impairment of LTP by corticosterone.CONCLUSION Taken together,this study demonstrates that hypofunction of NMDA receptors may be involved in impairment of LTP by corticosterone and reduced D-serine release may be an important reason for its hypofunction,which is an important complement to existing mechanisms of corticosterone-induced LTP and cognitive impairment. 展开更多
关键词 CORTICOSTERONE long-term potentiation N-methyl-D-aspartate receptors D-SERINE Na+-independent ala⁃nine-serine-cysteine transporter-1
下载PDF
Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer’s disease? 被引量:3
15
作者 Zhengtao Hu Tomas Ondrejcak +6 位作者 Pengpeng Yu Yangyang Zhang Yin Yang Igor Klyubin Sean P.Kennelly Michael J.Rowan Neng-Wei Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第6期1213-1219,共7页
Cognitive decline in Alzheimer’s disease correlates with the extent of tau pathology,in particular tau hyperphosphorylation that initially appears in the transentorhinal and related regions of the brain including the... Cognitive decline in Alzheimer’s disease correlates with the extent of tau pathology,in particular tau hyperphosphorylation that initially appears in the transentorhinal and related regions of the brain including the hippocampus.Recent evidence indicates that tau hyperphosphorylation caused by either amyloid-βor long-term depression,a form of synaptic weakening involved in learning and memory,share similar mechanisms.Studies from our group and others demonstrate that long-term depression-inducing low-frequency stimulation triggers tau phosphorylation at different residues in the hippocampus under different experimental conditions including aging.Conversely,certain forms of long-term depression at hippocampal glutamatergic synapses require endogenous tau,in particular,phosphorylation at residue Ser396.Elucidating the exact mechanisms of interaction between tau and long-term depression may help our understanding of the physiological and pathological functions of tau/tau(hyper)phosphorylation.We first summarize experimental evidence regarding tau-long-term depression interactions,followed by a discussion of possible mechanisms by which this interplay may influence the pathogenesis of Alzheimer’s disease.Finally,we conclude with some thoughts and perspectives on future research about these interactions. 展开更多
关键词 aging Alzheimer’s disease amyloid-β Aβoligomers HIPPOCAMPUS long-term depression long-term potentiation LTD ltp metabotropic glutamate receptor N-methyl-D-aspartate receptor tau hyperphosphorylation tau phosphorylation TAU
下载PDF
慢性应激对大鼠学习记忆能力和海马LTP的影响 被引量:24
16
作者 马强 王静 +2 位作者 杨志华 刘洪涛 晁福寰 《中国应用生理学杂志》 CAS CSCD 2000年第4期318-320,共3页
目的和方法 :本研究采用一种多因素的 2 1d慢性应激动物模型 ,以Y迷宫和LTP为指标 ,探讨慢性应激对动物学习记忆能力和海马神经突触可塑性的影响。结果 :长期慢性应激使大鼠空间学习记忆能力下降 ,而且 ,使中枢海马齿状回LTP的诱生受到... 目的和方法 :本研究采用一种多因素的 2 1d慢性应激动物模型 ,以Y迷宫和LTP为指标 ,探讨慢性应激对动物学习记忆能力和海马神经突触可塑性的影响。结果 :长期慢性应激使大鼠空间学习记忆能力下降 ,而且 ,使中枢海马齿状回LTP的诱生受到抑制。结论 :慢性应激可能使大鼠海马齿状回神经突触可塑性降低 。 展开更多
关键词 慢性应激 海马 长时程增强 学习记忆 ltp
下载PDF
微波辐照对大鼠学习记忆行为和海马LTP影响 被引量:8
17
作者 张彦文 安晓静 +2 位作者 谢燕 余争平 张广斌 《中国公共卫生》 CAS CSCD 北大核心 2007年第2期190-192,共3页
目的研究微波辐照后学习记忆功能与长时程增强(LTP)改变的规律。方法采用功率密度为65mW/cm2的微波全身一次辐照大鼠20 min,在辐照后不同时相点观察大鼠学习记忆行为的改变(穿梭箱试验和Morris水迷宫试验)和海马离体脑片LTP的诱导变化... 目的研究微波辐照后学习记忆功能与长时程增强(LTP)改变的规律。方法采用功率密度为65mW/cm2的微波全身一次辐照大鼠20 min,在辐照后不同时相点观察大鼠学习记忆行为的改变(穿梭箱试验和Morris水迷宫试验)和海马离体脑片LTP的诱导变化。结果微波辐照可导致大鼠肛温升高4.1℃,比吸收率(SAR)为12.0 W/kg。微波辐照后0,24 h,大鼠主动回避反应(AAR)明显低于辐照前(P<0.05)。微波辐照后0 h和3 h,大鼠寻找平台的潜伏期明显增加(P均<0.05);空间搜索试验中辐照组大鼠在目标区域的游泳时间占整个游泳时间的百分比和跨跃平台次数均显著低于对照组大鼠(P均<0.01)。微波辐照后0,12,24 h,3 d,大鼠海马脑片LTP的诱导明显减弱(0 h,P<0.01;12,24 h,3 d,P<0.05)。结论在本实验条件下,微波辐照可导致大鼠空间学习记忆能力受损,海马脑区LTP的诱导障碍是大鼠学习记忆功能损害的细胞电生理学基础。 展开更多
关键词 微波 学习记忆 海马 长时程增强
下载PDF
Treadmill exercise improves hippocampal neural plasticity and relieves cognitive deficits in a mouse model of epilepsy 被引量:2
18
作者 Hang Yu Mingting Shao +4 位作者 Xi Luo Chaoqin Pang Kwok-Fai So Jiandong Yu Li Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期657-662,共6页
Epilepsy frequently leads to cognitive dysfunction and approaches to treatment remain limited.Although regular exercise effectively improves learning and memory functions across multiple neurological diseases,its appl... Epilepsy frequently leads to cognitive dysfunction and approaches to treatment remain limited.Although regular exercise effectively improves learning and memory functions across multiple neurological diseases,its application in patients with epilepsy remains controversial.Here,we adopted a 14-day treadmill-exercise paradigm in a pilocarpine injection-induced mouse model of epilepsy.Cognitive assays confirmed the improvement of object and spatial memory after endurance training,and electrophysiological studies revealed the maintenance of hippocampal plasticity as a result of physical exercise.Investigations of the mechanisms underlying this effect revealed that exercise protected parvalbumin interneurons,probably via the suppression of neuroinflammation and improved integrity of blood-brain barrier.In summary,this work identified a previously unknown mechanism through which exercise improves cognitive rehabilitation in epilepsy. 展开更多
关键词 blood-brain barrier COGNITION HIPPOCAMPUS INTERNEURONS long-term potentiation microglial cell NEUROINFLAMMATION spatial memory temporal epilepsy treadmill exercise
下载PDF
开心散改善Aβ_(1-42)所致在体小鼠海马LTP抑制的实验研究 被引量:13
19
作者 黄树明 任丽民 +2 位作者 李健英 张博 范越 《中医药信息》 2013年第6期61-63,共3页
目的:观察开心散改善Aβ1-42对小鼠记忆以及海马LTP的抑制作用。方法:ICR小鼠随机分为正常对照组,Aβ组及Aβ加开心散组,实验组小鼠侧脑室注入Aβ1-42,对照组注射等体积生理盐水。Aβ加开心散组小鼠灌胃开心散,另外两组灌胃生理盐水进... 目的:观察开心散改善Aβ1-42对小鼠记忆以及海马LTP的抑制作用。方法:ICR小鼠随机分为正常对照组,Aβ组及Aβ加开心散组,实验组小鼠侧脑室注入Aβ1-42,对照组注射等体积生理盐水。Aβ加开心散组小鼠灌胃开心散,另外两组灌胃生理盐水进行对照。来用跳台法检测其学习记忆功能、动物活体记录其海马突触fEPSP分析其LTP。结果:Aβ组小鼠学习记忆功能及LTP明显抑制,Aβ加开心散组小鼠学习记忆功能及LTP明显改善。结论:开心散可改善Aβ1-42诱导的LTP抑制,从而改善动物记忆能力。 展开更多
关键词 淀粉样蛋白 长时程增强 u1P
下载PDF
慢性染铅对海马CA1区LTP及ERK2活性影响 被引量:6
20
作者 杨菁 孙黎光 +2 位作者 宗志宏 蔡葵 杜玉鑫 《中国公共卫生》 CAS CSCD 北大核心 2004年第1期21-22,共2页
目的 探讨慢性染铅对海马CA1区LTP及ERK2活性的影响。方法 用同心圆电极刺激海马的Schaffer侧支 ,于CA1区用细胞外玻璃电极记录单脉冲刺激引起的群峰电位 (PS) ,观察对照组和染铅组大鼠于高频刺激后PS幅值的变化 ;同时利用WesternBlot... 目的 探讨慢性染铅对海马CA1区LTP及ERK2活性的影响。方法 用同心圆电极刺激海马的Schaffer侧支 ,于CA1区用细胞外玻璃电极记录单脉冲刺激引起的群峰电位 (PS) ,观察对照组和染铅组大鼠于高频刺激后PS幅值的变化 ;同时利用WesternBlots方法检测海马CA1区ERK2的活性。结果 HFS前记录的对照组和染铅组的PS幅值无显著性差异 ;HFS后染铅组的PS平均幅值与对照组相比下降了 79% (P <0 0 1) ;染铅组CA1区的ERK2的活性比对照组下降了 2 4 1% (P <0 0 1)。结论 慢性染铅可抑制CA1-LTP的形成 。 展开更多
关键词 长时程增强 细胞外信号调节激酶2 海马
下载PDF
上一页 1 2 8 下一页 到第
使用帮助 返回顶部