检索结果-南通市图书馆

synaptic INPUTS FROM RODS AND CONES TO HORIZONTAL CELLS IN THE TIGER SALAMANDER RETINA

在线全文

学校读者我要写书评

暂无评论

Science China Chemistry 1990年第8期33卷 946-954页

作者：杨雄里 WU SAMUEL M. Shanghai Institute of Physiology Academia Sinica Shanghai 200031 PRC Cullen Eye Institute Baylor College of Medicins Houston Texas 77030 USA

synaptic inputs from rods and cones to horizontal cells (HCs) were studied in the flatmounted isolated retinas of the tiger salamander. Voltage-intensity relations, spectral sensitivities and response waveforms of the rod, the cone, and the HC under dark- and light-adapted conditions were examined. HCs receive mixed inputs from rods and cones in both dark- and light-adapted retinas. The relative rod/cone input in HC_s depends on the intensity of stimulus and background illumination, and it varies from HC to HC.

关键词： retina horizontal cells photoreceptor cells synaptic inputs

Two-dimensional materials for synaptic electronics and neuromorphic systems

在线全文

学校读者我要写书评

暂无评论

Science Bulletin 2019年第15期64卷 1056-1066页

作者： Shuiyuan Wang David Wei Zhang Peng Zhou State Key Laboratory of ASIC and System School of Microelectronics Fudan University

Synapses in biology provide a variety of functions for the neural system. Artificial synaptic electronics that mimic the biological neuron functions are basic building blocks and developing novel artificial synapses is essential for neuromorphic computation. Inspired by the unique features of biological synapses that the basic connection components of the nervous system and the parallelism, low power consumption, fault tolerance, self-learning and robustness of biological neural systems, artificial synaptic electronics and neuromorphic systems have the potential to overcome the traditional von Neumann bottleneck and create a new paradigm for dealing with complex problems such as pattern recognition, image classification, decision making and associative learning. Nowadays, two-dimensional(2 D) materials have drawn great attention in simulating synaptic dynamic plasticity and neuromorphic computing with their unique properties. Here we describe the basic concepts of bio-synaptic plasticity and learning, the 2 D materials library and its preparation. We review recent advances in synaptic electronics and artificial neuromorphic systems based on 2 D materials and provide our perspective in utilizing 2 D materials to implement synaptic electronics and neuromorphic systems in hardware.

关键词： Artificial synaptic electronics Neuromorphic computation 2D materials synaptic plasticity Hebbian learning

Rac1 Modulates Excitatory synaptic Transmission in Mouse Retinal Ganglion Cells

在线全文

学校读者我要写书评

暂无评论

Neuroscience Bulletin 2019年第4期35卷 673-687页

作者： Ling-Zhu Li Ning Yin Xue-Yan Li Yanying Miao Shuo Cheng Fang Li Guo-Li Zhao Shu-Min Zhong Xin Wang Xiong-Li Yang Zhongfeng Wang Department of Neurology Institutes of Brain Science State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Zhongshan Hospital Fudan University

Ras-related C3 botulinum toxin substrate 1(Racl),a member of the Rho GTPase family which plays important roles in dendritic spine morphology and plasticity,is a key regulator of cytoskeletal reorganization in dendrites and ***,we investigated whether and how Racl modulates synaptic transmission in mouse retinal ganglion cells(RGCs)using selective conditional knockout of Racl(Racl-cKO).Racl-cKO significantly reduced the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents,while glycine/GABA_A receptor-mediated miniature inhibitory postsynaptic currents were not *** the total GluA1 protein level was increased in Racl-cKO mice,its expression in the membrane component was *** did not affect spine-like branch density in single dendrites,but significantly reduced the dendritic complexity,which resulted in a decrease in the total number of dendritic spine-like *** results suggest that Racl selectively affects excitatory synaptic transmission in RGCs by modulating dendritic complexity.

关键词： Rac1 Retinal ganglion cell Excitatory synaptic transmission Dendrite Dendritic spine

PINK1-mediated Drp1^(S616) phosphorylation modulates synaptic development and plasticity via promoting mitochondrial fission

在线全文

学校读者我要写书评

暂无评论

Signal Transduction and Targeted Therapy 2022年第5期7卷 1719-1734页

作者： Qingtao Gao Runyi Tian Hailong Han Jesse Slone Caifang Wang Xiao Ke Tongmei Zhang Xiangyu Li Yuhong He Panlin Liao Fang Wang Ye Chen Shiqing Fu Kexuan Zhang Fangfang Zeng Yingxuan Yang Zhuo Li Jieqiong Tan Jiada Li Youming Lu Taosheng Huang Zhonghua Hu Zhuohua Zhang Institute of Molecular Precision Medicine Xiangya HospitalKey Laboratory of Molecular Precision Medicine of Hunan Province and Center for Medical GeneticsHunan Key Laboratory of Medical GeneticsCentral South UniversityChangshaHunan 410008China Department of Pediatrics Jacobs School of Medicine and Biomedical SciencesUniversity at BuffaloBuffaloNew York 14203USA Department of Physiology School of Basic Medicine and Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China The Institute for Brain Research Collaborative Innovation Center for Brain ScienceHuazhong University of Science and TechnologyWuhanHubei 430030China Hunan Key Laboratory of Animal Models for Human Diseases School of Life SciencesCentral South UniversityChangshaHunan 410008China Department of Neurosciences University of South China Medical SchoolHengyangHunan 421001China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangshaHunan 410008China Department of Critical Care Medicine Hunan Provincial Clinical Research Center for Critical Care MedicineXiangya HospitalCentral South UniversityChangshaHunan 410008China

Dynamic change of mitochondrial morphology and distribution along neuronal branches are essential for neural circuitry formation and synaptic ***,the underlying mechanism remains *** show here that Pink1 knockout(KO)mice display defective dendritic spine maturation,reduced axonal synaptic vesicles,abnormal synaptic connection,and attenuated long-term synaptic potentiation(LTP).Drp1 activation via ^(S616) phosphorylation rescues deficits of spine maturation in Pink1 KO neurons.

关键词： plasticity activation synaptic

ATP11B deficiency leads to impairment of hippocampal synaptic plasticity

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Journal of Molecular Cell Biology 2019年第8期11卷 688-702页

作者： Jiao Wang Weihao Li Fangfang Zhou Ruili Feng Fushuai Wang Shibo Zhang Jie Li Qian Li Yajiang Wang Jiang Xie Tieqiao Wen Laboratory of Molecular Neural Biology School of Life Sciences Shanghai University Shanghai 200444 China School of Computer Engineering and Science Shanghai University Shanghai 200444 China

synaptic plasticity is known to regulate and support signal transduction between neurons, while synaptic dysfunction contributes to multiple neurological and other brain disorders;however, the specific mechanism underlying this process remains unclear. In the present study, abnormal neural and dendritic morphology was observed in the hippocampus following knockout of Atpllb both in vitro and in vivo. Moreover, ATP11B modified synaptic ultrastructure and promoted spine remodeling via the asymmetrical distribution of phosphatidylserine and enhancement of glutamate release, glutamate receptor expression, and intracellular Ca^2+ concentration. Fuithermoe experimental results also indicate that ATP11B regulated synaptic plasticity in hippocampal neurons through the MAPK14 signaling pathway. In conclusion, our data shed light on the possible mechanisms underlying the regulation of synaptic plasticity and lay the foundation for the exploration of proteins involved in signal transduction during this process.

关键词： ATP11B synaptic plasticity glutamate receptors MAPK14 signaling pathway

Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2019年第6期14卷 1037-1045页

作者： Ning Li Yang Li Li-Juan Li Ke Zhu Yan Zheng Xiao-Min Wang Department of Neurobiology Capital Medical University Key Laboratory for Neurodegenerative Disorders of the Ministry of Education Capital Medical University Beijing Institute for Brain Disorders Department of Physiology Capital Medical University

Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer's disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer's disease remain unclear. In the present study, Alzheimer's disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer's disease-like diseases. APP/PS1 double transgenic(5 XFAD; Jackson Laboratory) mice and their littermates(wild-type, controls) were used in this study. Additional 6-weekold and 10-week-old 5 XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For10-week-old 5 XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5 XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5 XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer's disease. The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Ca

关键词： nerve regeneration Alzheimer’s disease synaptic plasticity hippocampus learning and memory long-term potentiation βamyloid glutamate receptor synaptic strength neural regeneration

Paired associative stimulation improves synaptic plasticity and functional outcomes after cerebral ischemia

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2019年第11期14卷 1968-1976页

作者： Yan Hu Tie-Cheng Guo Xiang-Yu Zhang Jun Tian Yin-Shan Lu Department of Rehabilitation Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science & TechnologyWuhanHubei ProvinceChina Department of Rehabilitation Medicine Zhongnan Hospital of Wuhan UniversityWuhanHubei ProvinceChina Department of Rehabilitation Medicine the Fifth Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina

Paired associative stimulation is a relatively new non-invasive brain stimulation technique that combines transcranial magnetic stimulation and peripheral nerve stimulation. The effects of paired associative stimulation on the excitability of the cerebral cortex can vary according to the time interval between the transcranial magnetic stimulation and peripheral nerve stimulation. We established a model of cerebral ischemia in rats via transient middle cerebral artery occlusion. We administered paired associative stimulation with a frequency of 0.05 Hz 90 times over 4 weeks. We then evaluated spatial learning and memory using the Morris water maze. Changes in the cerebral ultra-structure and synaptic plasticity were assessed via transmission electron microscopy and a 64-channel multi-electrode array. We measured mRNA and protein expression levels of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 in the hippocampus using a real-time polymerase chain reaction and western blot assay. Paired associative stimulation treatment significantly improved learning and memory in rats subjected to cerebral ischemia. The ultra-structures of synapses in the CA1 area of the hippocampus in rats subjected to cerebral ischemia were restored by paired associative stimulation. Long-term potentiation at synapses in the CA3 and CA1 regions of the hippocampus was enhanced as well. The protein and mRNA expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 increased after paired associative stimulation treatment. These data indicate that paired associative stimulation can protect cog-nition after cerebral ischemia. The observed effect may be mediated by increases in the mRNA and protein expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1, and by enhanced synaptic plasticity in the CA1 area of the hippocampus. The animal experiments were approved by the Animal Ethics Committee of Tongji Medical College, Huazhon

关键词： cerebral ischemia paired associative stimulation cognitive function long-term potentiation synaptic plasticity Morris water maze synaptic structure N-methyl-D-aspartic acid receptor brain-derived neurotrophic factor multi-electrode array neural regeneration

AVP(4-8) Improves Cognitive Behaviors and Hippocampal synaptic Plasticity in the APP/PS1 Mouse Model of Alzheimer’s Disease

在线全文

学校读者我要写书评

暂无评论

Neuroscience Bulletin 2020年第3期36卷 254-262页

作者： Xiumin Zhang Fang Zhao Chenfang Wang Jun Zhang Yu Bai Fang Zhou Zhaojun Wang Meina Wu Wei Yang Junhong Guo Jinshun Qi Department of Neurology First HospitalShanxi Medical UniversityTaiyuan 030001China Department of Physiology Key laboratory of Cellular PhysiologyMinistry of EducationShanxi Medical UniversityTaiyuan 030001China

Memory deficits with aging are related to the neurodegeneration in the brain, including a reduction in arginine vasopressin(AVP) in the brain of patients with Alzheimer’s disease(AD). AVP(4-8), different from its precursor AVP, plays memory enhancement roles in the CNS without peripheral side-effects. However, it is not clear whether AVP(4-8) can improve cognitive behaviors and synaptic plasticity in the APP/PS1 mouse model of AD. Here, we investigated for the first time the neuroprotective effects of AVP(4-8) on memory behaviors and in vivo long-term potentiation(LTP) in APP/PS1-AD *** results showed that:(1) APP/PS1-AD mice had lower spontaneous alternation in the Y-maze than wild-type(WT) mice, and this was significantly reversed by AVP(4-8);(2) the prolonged escape latency of APP/PS1-AD mice in the Morris water maze was significantly decreased by AVP(4-8), and the decreased swimming time in target quadrant recovered significantly after AVP(4-8) treatment;(3) in vivo hippocampal LTP induced by high-frequency stimulation had a significant deficit in the AD mice, and this was partly rescued by AVP(4-8);(4) AVP(4-8)significantly up-regulated the expression levels of postsynaptic density 95(PSD95) and nerve growth factor(NGF)in the hippocampus of AD mice. These results reveal the beneficial effects of AVP(4-8) in APP/PS1-AD mice,showing that the intranasal administration of AVP(4-8)effectively improved the working memory and long-term spatial memory of APP/PS1-AD mice, which may be associated with the elevation of PSD95 and NGF levels in the brain and the maintenance of hippocampal synaptic plasticity.

关键词： AVP(4-8) APP/PS1 transgenic mice Cognitive behavior synaptic plasticity In vivo hippocampal LTP

An enriched environment promotes synaptic plasticity and cognitive recovery after permanent middle cerebral artery occlusion in mice

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2019年第3期14卷 462-469页

作者： Chuan-Jie Wang Yi Wu Qun Zhang Ke-Wei Yu Yu-Yang Wang Department of Rehabilitation Medicine Huashan Hospital Fudan University

Cerebral ischemia activates an endogenous repair program that induces plastic changes in neurons. In this study, we investigated the effects of environmental enrichment on spatial learning and memory as well as on synaptic remodeling in a mouse model of chronic cerebral ischemia, produced by subjecting adult male C57 BL/6 mice to permanent left middle cerebral artery occlusion. Three days postoperatively, mice were randomly assigned to the environmental enrichment and standard housing groups. Mice in the standard housing group were housed and fed a standard diet. Mice in the environmental enrichment group were housed in a cage with various toys and fed a standard diet. Then, 28 days postoperatively, spatial learning and memory were tested using the Morris water maze. The expression levels of growth-associated protein 43, synaptophysin and postsynaptic density protein 95 in the hippocampus were analyzed by western blot assay. The number of synapses was evaluated by electron microscopy. In the water maze test, mice in the environmental enrichment group had a shorter escape latency, traveled markedly longer distances, spent more time in the correct quadrant(northeast zone), and had a higher frequency of crossings compared with the standard housing group. The expression levels of growth-associated protein 43, synaptophysin and postsynaptic density protein 95 were substantially upregulated in the hippocampus in the environmental enrichment group compared with the standard housing group. Furthermore, electron microscopy revealed that environmental enrichment increased the number of synapses in the hippocampal CA1 region. Collectively, these findings suggest that environmental enrichment ameliorates the spatial learning and memory impairment induced by permanent middle cerebral artery occlusion. Environmental enrichment in mice with cerebral ischemia likely promotes cognitive recovery by inducing plastic changes in synapses.

关键词： nerve regeneration environmental enrichment cerebral ischemia cognitive recovery brain plasticity and reorganization synaptic plasticity electron microscopy growth-associated protein 43 synaptophysin postsynaptic density protein 95 permanent middle cerebral artery occlusion neural regeneration