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Constraint-induced movement therapy enhances AMPA receptor-dependent synaptic plasticity in the ipsilateral hemisphere following ischemic stroke

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Neural Regeneration Research 2021年第2期16卷 319-324页

作者： Jian Hu Pei-Le Liu Yan Hua Bei-Yao Gao Yu-Yuan Wang Yu-Long Bai Chan Chen Department of Rehabilitation Medicine Huashan HospitalFudan UniversityShanghaiChina

Constraint-induced movement therapy(CIMT)can promote the recovery of motor function in injured upper limbs following stroke,which may be associated with upregulation ofα-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor(AMPAR)at synapses in the ipsilateral sensorimotor cortex in our previous study.However,AMPAR distribution is tightly regulated,and only AMPARs on the postsynaptic membrane can mediate synaptic transmission.We speculated that synaptic remodeling induced by movement-associated synaptic activity can promote functional recovery from stroke.To test this hypothesis,we compared AMPAR expression on the postsynaptic membrane surface in a rat model of ischemic stroke induced by middle cerebral artery occlusion(MCAO)with versus without CIMT,which consisted of daily running wheel training for 2 weeks starting on day 7 after MCAO.The results showed that CIMT increased the number of glutamate receptor(Glu R)2-containing functional synapses in the ipsilateral sensorimotor cortex,and reduced non-Glu R2 AMPARs in the ipsilateral sensorimotor cortex and hippocampal CA3 region.In addition,CIMT enhanced AMPAR expression on the surface of post-synaptic membrane in the ipsilateral sensorimotor cortex and hippocampus.Thus,CIMT promotes the recovery of motor function of injured upper limbs following stroke by enhancing AMPAR-mediated synaptic transmission in the ischemic hemisphere.These findings provide supporting evidence for the clinical value of CIMT for restoring limb movement in stroke patients.All experimental procedures and protocols were approved by the Department of Laboratory Animal Science of Fudan University,China(approval No.201802173 S)on March 3,2018.

关键词： brain experiment injury plasticity regeneration repair stroke synapse

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The neuro-glial coagulonome: the thrombin receptor and coagulation pathways as major players in neurological diseases

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Neural Regeneration Research 2019年第12期14卷 2043-2053页

作者： Shany G.Gofrit Efrat Shavit-Stein Department of Neurology and Joseph Sagol Neuroscience Center Sheba Medical Center Tel Hashomer Sackler Faculty of Medicine Tel Aviv University

The neuro-glial interface extends far beyond mechanical support alone and includes interactions through coagulation cascade proteins. Here, we systematically review the evidence indicating that synaptic and node of Ranvier glia cell components modulate synaptic transmission and axonal conduction by a coagulation cascade protein system, leading us to propose the concept of the neuro-glial coagulonome. In the peripheral nervous system, the main thrombin receptor protease activated receptor 1 (PAR1) is located on the Schwann microvilli at the node of Ranvier and at the neuromuscular junction. PAR1 activation effects can be both neuroprotective or harmful, depending on thrombin activity levels. Low physiological levels of thrombin induce neuroprotective effects in the Schwann cells which are mediated by the endothelial protein C receptor. High levels of thrombin induce conduction deficits, as found in experimental autoimmune neuritis, the animal model for Guillaine-Barre syndrome. In the central nervous system, PAR1 is located on the peri-synaptic astrocyte end-feet. Its activation by high thrombin levels is involved in the pathology of primary inflammatory brain diseases such as multiple sclerosis, as well as in other central nervous system insults, including trauma, neoplasms, epilepsy and vascular injury. Following activation of PAR1 by high thrombin levels the seizure threshold is lowered. On the other hand, PAR1 activation by lower levels of thrombin in the central nervous system protects against a future ischemic insult. This review presents the known structure and function of the neuro-glial coagulonome, focusing on coagulation, thrombin and PAR1 in a pathway which may be either physiological (neuroprotective) or detrimental in peripheral nervous system and central nervous system diseases. Understanding the neuro-glial coagulonome may open opportunities for novel pharmacological interventions in neurological diseases.

关键词： thrombin protease activated receptor 1 protease nexin 1 glia node of Ranvier synapse epilepsy glioblastoma Guillaine-Barre syndrome

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Thrombospondin 1 promotes synaptic formation in bone marrow-derived neuron-like cells

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Neural Regeneration Research 2013年第10期8卷 869-881页

作者： Yun Huang Mingnan Lu Weitao Guo Rong Zeng Bin Wang Huaibo Wang Department of Orthopedics Affiliated Hospital of Guangdong Medical College

In this study, a combination of growth factors was used to induce bone marrow mesenchymal stem cells differentiation into neuron-like cells, in a broader attempt to observe the role of thrombospondin 1 in synapse formation. Results showed that there was no significant difference in the differentiation rate of neuron-like cells between bone marrow mesenchymal stem cells with thrombospondin induction and those without. However, the cell shape was more complex and the neurites were dendritic, with unipolar, bipolar or multipolar morphologies, after induction with thrombospondin 1. The induced cells were similar in morphology to normal neurites. Immunohistochemical staining showed that the number of positive cells for postsynaptic density protein 95 and synaptophysin 1 protein was significantly increased after induction with thrombospondin 1. These findings indicate that thrombospondin 1 promotes synapse formation in neuron-like cells that are differentiated from bone marrow mesenchymal stem cells.

关键词： neural regeneration stem cells bone marrow mesenchymal stem cells neuron-like cells synapse thrombospondin 1 neurite postsynaptic density protein 95 synaptophysin 1 neuron-specificenolase glial fibrillary acidic protein grants-supported paper neuroregeneration

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Synaptic aging disrupts synaptic morphology and function in cerebellar Purkinje cells

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Neural Regeneration Research 2018年第6期13卷 1019-1025页

作者： Wen-Juan Fan Ming-Chao Yan Lai Wang Yi-Zheng Sun Jin-Bo Deng Jie-Xin Deng Institute of Neurobiology School of Life Science Henan University

synapses are key structures in neural networks,and are involved in learning and memory in the central nervous system.Investigating synaptogenesis and synaptic aging is important in understanding neural development and neural degeneration in diseases such as Alzheimer disease and Parkinson’s disease.Our previous study found that synaptogenesis and synaptic maturation were harmonized with brain development and maturation.However,synaptic damage and loss in the aging cerebellum are not well understood.This study was designed to investigate the occurrence of synaptic aging in the cerebellum by observing the ultrastructural changes of dendritic spines and synapses in cerebellar Purkinje cells of aging mice.Immunocytochemistry,Di I diolistic assays,and transmission electron microscopy were used to visualize the morphological characteristics of synaptic buttons,dendritic spines and synapses of Purkinje cells in mice at various ages.With synaptic aging in the cerebellum,dendritic spines and synaptic buttons were lost,and the synaptic ultrastructure was altered,including a reduction in the number of synaptic vesicles and mitochondria in presynaptic termini and smaller thin specialized zones in pre-and post-synaptic membranes.These findings confirm that synaptic morphology and function is disrupted in aging synapses,which may be an important pathological cause of neurodegenerative diseases.

关键词： nerve regeneration aging cerebellum degenerative disease dendritic spine nerve regeneration mice neurodegenerative diseases Purkinje cells synapse synaptogenesis synaptic ultrastructure neural regeneration

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Increased hippocampal Disrupted-In-Schizophrenia 1 expression in mice exposed prenatally to lead

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Neural Regeneration Research 2012年第25期7卷 1939-1945页

作者： Yuanyuan You Liguang Sun Bo Peng Yan Li Songbin Ben Shuang Gao Department of Biochemical and Molecular Biology China Medical University Shenyang 110001 Liaoning Province China Outpatient Department of China Medical University Shenyang 110001 Liaoning Province China Department of Biochemical and Molecular Biology Jilin Medical College Jilin 132013 Jilin Province China School of Life Science Liaoning University Shenyang 110036 Liaoning Province China School of Public Health China Medical University Shenyang 110001 Liaoning Province China

Disrupted-in-Schizophrenia 1 is a susceptibility gene for schizophrenia and other psychiatric disorders. Developmental lead exposure can cause neurological disorders similar to hyperactivity disorder, dyslexia and schizophrenia. In the present study, we examined the impact of developmental lead exposure, administered in vitro and in vivo, on hippocampal Disrupted-In- Schizophrenia 1 expression. Our results show that in cultured hippocampal neurons, in vitro exposure to 0.1-10 pM lead, inhibited neurite growth and increased Disrupted-In-Schizophrenia 1 mRNA and protein expression dose-dependently. In addition, blood lead levels in mice were increased with increasing mouse maternal lead （0.01-1 mM） exposure. Hippocampal neurons from these mice showed a concomitant increase in Disrupted-in-Schizophrenia 1 mRNA and protein expression. Overall our findings suggest that in vivo and in vitro lead exposure increases Disrupted-In-Schizophrenia 1 expression in hippocampal neurons dose-dependently, and consequently may influence synapse formation in newborn neurons.

关键词： lead exposure Disrupted-In-Schizophrenia 1 hippocampus neuron neurotoxicity synapse neuralregeneration

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Role of the PTEN signaling pathway in autism spectrum disorder

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Neuroscience Bulletin 2013年第6期29卷 773-778页

作者： Jing-Wen Lv Tian-Lin Cheng Zi-Long Qiu Wen-Hao Zhou Department of Neonatology Children's Hospital of Fudan University Institute of Neuroscience Shanghai Institute of Biological SciencesChinese Academy of Sciences

Autism is an etiologically heterogeneous group of neurodevelopmental disorders,diagnosed mostly by the clinical behavioral phenotypes.The concept that the tumor-related gene PTEN plays a critical role in autism spectrum disorder has emerged over the last decade.In this review,we focus on the essential role of the PTEN signaling pathway in neuronal differentiation and the formation of neural circuitry,as well as genetic mouse models with Pten manipulations.Particularly,accumulated data suggest that the effect of PTEN on neural stem-cell development contributes significantly to the pathophysiology of autism spectrum disorders.

关键词： PTEN TSC1/2 autism synapse neural stem cells

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Astaxanthin alleviates pathological brain aging through the upregulation of hippocampal synaptic proteins

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Neural Regeneration Research 2021年第6期16卷 1062-1067页

作者： Ning Liu Liang Zeng Yi-Ming Zhang Wang Pan Hong Lai Department of Human Anatomy College of Basic MedicineChina Medical UniversityShenyangLiaoning ProvinceChina Department of Radiology The First Affiliated Hospital of Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina Department of Human Anatomy College of Basic MedicineShenyang Medical CollegeShenyangLiaoning ProvinceChina Department of Neurobiology of Jinzhou Medical University JinzhouLiaoning ProvinceChina

Oxidative stress is currently considered to be the main cause of brain aging.Astaxanthin can improve oxidative stress under multiple pathological conditions.It is therefore hypothesized that astaxanthin might have therapeutic effects on brain aging.To validate this hypothesis and investigate the underlying mechanisms,a mouse model of brain aging was established by injecting amyloid beta(Aβ)25-35(5μM,3μL/injection,six injections given every other day)into the right lateral ventricle.After 3 days of Aβ25-35 injections,the mouse models were intragastrically administered astaxanthin(0.1 mL/d,10 mg/kg)for 30 successive days.Astaxanthin greatly reduced the latency to find the platform in the Morris water maze,increased the number of crossings of the target platform,and increased the expression of brain-derived neurotrophic factor,synaptophysin,sirtuin 1,and peroxisome proliferator-activated receptor-γ coactivator 1α.Intraperitoneal injection of the sirtuin 1 inhibitor nicotinamide(500μM/d)for 7 successive days after astaxanthin intervention inhibited these phenomena.These findings suggest that astaxanthin can regulate the expression of synaptic proteins in mouse hippocampus through the sirtuin 1/peroxisome proliferator-activated receptor-γcoactivator 1αsignaling pathway,which leads to improvements in the learning,cognitive,and memory abilities of mice.The study was approved by the Animal Ethics Committee,China Medical University,China(approval No.CMU2019294)on January 15,2019.

关键词： brain aging cognitive factor hippocampus learning memory oxidative stress pathways synapse

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Protective effects of Dendrobium nobile Lindl. alkaloids on amyloid beta(25–35)-induced neuronal injury

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Neural Regeneration Research 2017年第7期12卷 1131-1136页

作者： Wei Zhang Qin Wu Yan-liu Lu Qi-hai Gong Feng Zhang Jing-shan Shi Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry ofEducation Zunyi Medical University Zunyi Guizhou Province China

Dendrobium nobile Lindl.alkaloids（DNLA）,the active ingredients of a traditional Chinese medicine Dendrobium,have been shown to have anti-oxidative effects,anti-inflammatory action,and protective effect on neurons against oxygen-glucose deprivation.However,it is not clear whether DNLA reduces amyloid-beta（Aβ）-induced neuronal injury.In this study,cortical neurons were treated with DNLA at different concentrations（0.025,0.25,and 2.5 mg/L）for 24 hours,followed by administration of Aβ（25-35）（10μM）.Aβ（25-35） treatments increased cell injury as determined by the leakage of lactate dehydrogenase,which was accompanied by chromatin condensation and mitochondrial tumefaction.The damage caused by Aβ（25-35） on these cellular properties was markedly attenuated when cells were pretreated with DNLA.Treatment with Aβ（25-35）down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95,all changes were significantly reduced by pretreatment of cells with DNLA.These findings suggest that DNLA reduces the cytotoxicity induced by Aβ（25-35） in rat primary cultured neurons.The protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated,at least in part,through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.

关键词： nerve regeneration Dendrobium nobile Lindl. alkaloids amyloid beta neurons synapse synaptophysin postsynaptic density-95 cognitive impairment neuroprotection neural regeneration

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A mathematical model of synaptotagmin 7 revealing functional importance of short-term synaptic plasticity

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Neural Regeneration Research 2019年第4期14卷 621-631页

作者： Yao He Don Kulasiri Jingyi Liang Center for Advanced Computational Solutions (C-fACS) Lincoln UniversityChristchurch New Zealand

Synaptotagmin 7(Syt7), a presynaptic calcium sensor, has a significant role in the facilitation in shortterm synaptic plasticity: Syt7 knock out mice show a significant reduction in the facilitation. The functional importance of short-term synaptic plasticity such as facilitation is not well understood. In this study, we attempt to investigate the potential functional relationship between the short-term synaptic plasticity and postsynaptic response by developing a mathematical model that captures the responses of both wild-type and Syt7 knock-out mice. We then studied the model behaviours of wild-type and Syt7 knock-out mice in response to multiple input action potentials. These behaviors could establish functional importance of short-term plasticity in regulating the postsynaptic response and related synaptic properties. In agreement with previous modeling studies, we show that release sites are governed by non-uniform release probabilities of neurotransmitters. The structure of non-uniform release of neurotransmitters makes shortterm synaptic plasticity to act as a high-pass filter. We also propose that Syt7 may be a modulator for the long-term changes of postsynaptic response that helps to train the target frequency of the filter. We have developed a mathematical model of short-term plasticity which explains the experimental data.

关键词： synapse short-term plasticity short-term facilitation and depression mathematical model low-frequency stimulation high-frequency stimulation

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Effects of electromagnetic radiation on spatial memory and synapses in rat hippocampal CA1

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Neural Regeneration Research 2012年第16期7卷 1248-1255页

作者： Yuhong Li Changhua Shi Guobing Lu Qian Xu Shaochen Liu Chengde Medical University Chengde 067000 Hebei Province China

In this study, we investigated the effects of mobile phone radiation on spatial learning, reference memory, and morphology in related brain regions. After the near-field radiation （0.52 1.08 W/kg） was delivered to 8-week-old Wistar rats 2 hours per day for 1 month, behavioral changes were examined using the Morris water maze. Compared with the sham-irradiated rats, the irradiated rats exhibited impaired performance. Morphological changes were investigated by examining synaptic ultrastructural changes in the hippocampus. Using the physical dissector technique, the number of pyramidal neurons, the synaptic profiles, and the length of postsynaptic densities in the CA1 region were quantified stereologically. The morphological changes included mitochondrial degenerations, fewer synapses, and shorter postsynaptic densities in the radiated rats. These findings indicate that mobile phone radiation can significantly impair spatial learning and reference memory and induce morphological changes in the hippocampal CA1 region.

关键词： mobile phone memory Morris water maze electron microscopy synapse postsynaptic density quantitative analysis ultrastructure neural regeneration

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