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Thrombospondins and synaptogenesis

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Neural Regeneration Research 2012年第22期7卷 1737-1743页

作者： Bin Wang Weitao Guo Yun Huang Department of Orthopedics Affiliated Hospital of Guangdong Medical CollegeZhanjiang 524001Guangdong ProvinceChina

Here, we review research on the mechanisms underlying the ability of thrombospondin to promote synaptogenesis and examine its role in central nervous system diseases and drug actions. Thrombospondin secreted by glial cells plays a critical role in synaptogenesis and maintains synapse stability. Thrombospondin regulates synaptogenesis through receptor a26-1 and neuroligin 1, and promotes the proliferation and differentiation of neural progenitor cells. It also participates in synaptic remodeling following injury and in the action of some nervous system drugs.

关键词： thrombospondin synapse synaptogenesis glial cell α2δ-1 extracellular matrix neural progenitorcells Notch opioid regeneration neural regeneration

C-X-C chemokine receptor type 7 antibody enhances neural plasticity after ischemic stroke

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Neural Regeneration Research 2023年第9期18卷 1976-1982页

作者： Xiao-Qian Zhang Xiao-Yin Wang Bing-Chao Dong Mei-Xuan Li Yu Wang Ting Xiao Shan-Shan Zhao Department of Neurology The First Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Key Laboratory of Immunodermatology Ministry of HealthMinistry of EducationShenyangLiaoning ProvinceChina

Stromal cell-derived factor-1 and its receptor C-X-C chemokine receptor 4(CXCR4) have been shown to regulate neural regeneration after stroke.Howeve r,whether stromal cell-derived factor-1 receptor CXCR7,which is widely distributed in the develo ping and adult central nervous system,participates in neural regeneration remains poorly unde rstood.In this study,we established rat models of focal cerebral ischemia by injecting endothelin-1 into the cerebral co rtex and striatum.Starting on day 7 after injury,CXCR7-neutralizing antibody was injected into the lateral ventricle using a micro drug delivery system for 6 consecutive days.Our results showed that CXCR7-neutralizing antibody increased the total length and number of sprouting co rticospinal tra ct fibers in rats with cerebral ischemia,increased the expression of vesicular glutamate transporter 1 and growth-related protein 43,marke rs of the denervated spinal cord synapses,and promoted the differentiation and maturation of oligodendrocyte progenitor cells in the striatum.In addition,CXCR7 antibody increased the expression of CXCR4 in the striatum,increased the protein expression of RAS and ERK1/2 associated with the RAS/ERK signaling pathway,and im proved rat motor function.These findings suggest that CXCR7 improved neural functional recovery after ischemic stroke by promoting axonal regeneration,synaptogenesis,and myelin regeneration,which may be achieved by activation of CXCR4 and the RAS/ERK1/2 signaling pathway.

关键词： axonal regeneration cerebral ischemia C-X-C chemokine receptor 4 CXCR7 antibody neural plasticity RAS/ERK pathway remyelination stroke stromal cell-derived factor-1 synaptogenesis

Differentiation and functional connectivity of fetal tectal transplants

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Neural Regeneration Research 2023年第11期18卷 2325-2331页

作者： Alan R.Harvey School of Human Sciences The University of Western AustraliaLions Eye Instituteand Perron Institute for Neurological and Translational ScienceNedlandsWAAustralia

Data from studies analyzing the differentiation and functional connectivity of embryo nic neural tissue grafted into the mammalian nervous system has led to the clinical testing of the fetal graft approach in patients with neurodegenerative disease.While some success has been achieved,ethical concerns have led to a search for alternative therapeutic strategies,mostly exploring the use of neural precursors or neurons derived from pluripotent stem cells to replace damaged host neurons and restore lost circuitries.These more recent studies address questions of graft viability,differentiation,and connectivity similar to those posed by researchers in earlier fetal transplant work,thus reviews of the fetal graft literature may inform and help guide ongoing research in the stem cell/organoid field.This brief review describes some key observations from research into the transplantation of neural tissue into the rat visual syste m,focusing on grafts of the fetal supe rior colliculus(tectal grafts) into neonatal or adult hosts.In neonate hosts,grafts quickly develop connections with the underlying host mid b rain and attain a morphology typical of mature grafts by about 2 weeks.G rafts consistently contain numerous localized regions which,based on neurofibrillar staining,neuronal morphology(Golgi),neurochemistry,receptor expression,and glial architecture,are homologous to the stratum griseum supe rficiale of normal superior colliculus.These localized "patches" are also seen after explant culture and when donor tectal tissue is dissociated and reaggregated prior to transplantation.In almost all circumstances,host retinal innervation is restricted to these localized patches,but only those that are located adjacent to the graft surfa ce.Synapses are formed and there is evidence of functional drive.The only exception occurs when Schwann cells are added to dissociated tecta prior to reaggregation.In these co-grafts,the peripheral glia appear to compete with local target fa ctors and host retinal ingrowth is more widespread.Othe

关键词： axon regeneration differentiation embyronic grafts fetal tissue neural precursors retinotectal stem cells superior colliculus synaptogenesis transplantation

Neuronal guidance genes in health and diseases

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Protein & Cell 2023年第4期14卷 238-261页

作者： Junichi Yuasa-Kawada Mariko Kinoshita-Kawada Yoshio Tsuboi Jane Y.Wu Department of Neurology Fukuoka University7.451 NanakumaJohnan.kuFukuoka 814-0180Japan Department of Neurology Center for Genetic MedicineLurie Cancer CenterNorthwestern University Feinberg School of MedicineWard Building Box 6117303E.Chicago AvenueChicagoIlinois 60611.USA

Neurons migrate from their birthplaces to the destinations,and extending axons navigate to their synaptic targets by sensing various extracellular cues in spatiotemporally controlled manners.These evolutionally conserved guidance cues and their receptors regulate multiple aspects of neural development to establish the highly complex nervous system by mediating both short-and long-range cell-cell communications.Neuronal guidance genes(encoding cues,receptors,or downstream signal transducers)are critical not only for development of the nervous system but also for synaptic maintenance,remodeling,and function in the adult brain.One emerging theme is the combinatorial and complementary functions of relatively limited classes of neuronal guidance genes in multiple processes,including neuronal migration,axonal guidance,synaptogenesis,and circuit formation.Importantly,neuronal guidance genes also regulate cell migration and cell-cell communications outside the nervous system.We are just beginning to understand how cells integrate multiple guidance and adhesion signaling inputs to determine overall cellular/subcellular behavior and how aberrant guidance signaling in various cell types contributes to diverse human diseases,ranging from developmental,neuropsychiatric,and neurodegenerative disorders to cancer metastasis.We review classic studies and recent advances in understanding signaling mechanisms of the guidance genes as well as their roles in human diseases.Furthermore,we discuss the remaining chalienges and therapeutic potentials of modulating neuronal guidance pathways in neural repair.

关键词： axon guidance neuronal migration synaptogenesis neural circuit formation neural mapping cell-cell communications angiogenesis organogenesis cancermetastasis

Interactions Between Astrocytes and Oligodendroglia in Myelin Development and Related Brain Diseases

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Neuroscience Bulletin 2023年第3期39卷 541-552页

作者： Xuelian Hu Guangdan Yu Xiang Liao Lan Xiao School of Medicine Chongqing UniversityChongqing 400030China Department of Histology and Embryology Chongqing Key Laboratory of NeurobiologyBrain and Intelligence Research Key Laboratory of Chongqing Education CommissionThird Military Medical UniversityChongqing 400038China

Astrocytes(ASTs)and oligodendroglial lineage cells(OLGs)are major macroglial cells in the central nervous system.ASTs communicate with each other through connexin(Cx)and Cx-based network structures,both of which allow for quick transport of nutrients and signals.Moreover,ASTs interact with OLGs through connexin(Cx)-mediated networks to modulate various physiological processes in the brain.In this article,following a brief description of the infrastructural basis of the glial networks and exocrine factors by which ASTs and OLGs may crosstalk,we focus on recapitulating how the interactions between these two types of glial cells modulate myelination,and how the AST-OLG interactions are involved in protecting the integrity of the blood-brain barrier(BBB)and regulating synaptogenesis and neural activity.Recent studies further suggest that AST-OLG interactions are associated with myelin-related diseases,such as multiple sclerosis.A better understanding of the regulatory mechanisms underlying AST-OLG interactions may inspire the development of novel therapeutic strategies for related brain diseases.

关键词： Astrocyte Oligodendroglia Glial network Myelination synaptogenesis Neuroinfammation

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

Autophagy in synaptic development,function,and pathology

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Neuroscience Bulletin 2015年第4期31卷 416-426页

作者： Dan-Na Shen Li-Hui Zhang Er-Qing Wei Yi Yang Department of Pharmacology Hangzhou Key Laboratory of Medical NeurobiologySchool of MedicineHangzhou Normal University Department of Pharmacology Zhejiang University School of Medicine

In the nervous system, neurons contact each other to form neuronal circuits and drive behavior, relying heavily on synaptic connections. The proper development and growth of synapses allows functional transmission of electrical information between neurons or between neurons and muscle fibers. Defects in synapse-formation or development lead to many diseases. Autophagy, a major determinant of protein turnover, is an essential process that takes place in developing synapses. During the induction of autophagy, proteins and cytoplasmic components are encapsulated in autophagosomes, which fuse with lysosomes to form autolysosomes. The cargoes are subsequently degraded and recycled. However, aberrant autophagic activity may lead to synaptic dysfunction, which is a common pathological characteristic in several disorders. Here, we review the current understanding of autophagy in regulating synaptic development and function. In addition, autophagy-related synaptic dysfunction in human diseases is also summarized.

关键词： autophagy synaptogenesis synaptic elimination synaptic function synaptic pathology

Matrine promotes neural circuit remodeling to regulate motor function in a mouse model of chronic spinal cord injury

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Neural Regeneration Research 2019年第11期14卷 1961-1967页

作者： Norio Tanabe Tomoharu Kuboyama Chihiro Tohda Division of Neuromedical Science Institute of Natural Medicine University of Toyama

In chronic phase of spinal cord injury, functional recovery is more untreatable compared with early intervention in acute phase of spinal cord injury. In the last decade, several combination therapies successfully improved motor dysfunction in chronic spinal cord injury. However, their effectiveness is not sufficient. We previously found a new effective compound for spinal cord injury, matrine, which induced axonal growth and functional recovery in acute spinal cord injury mice via direct activation of extracellular heat shock protein 90. Although our previous study clarified that matrine was an activator of extracellular heat shock protein 90, the potential of matrine for spinal cord injury in chronic phase has not been sufficiently evaluated. Thus, this study aimed to investigate whether matrine ameliorates chronic spinal cord injury in mice. Once daily intragastric administration of matrine(100 μmol/kg per day) to spinal cord injury mice were starte at 28 days after injury, and continued for 154 days. Continuous mat rine treatment improved hindlimb motor function in chronic spinal cord injury mice. In injured spinal cords of the matrine-treated mice, the density of neurofilament-H-positive axons was increased. Moreover, matrine treatment increased the density of bassoon-positive presynapses in contact with choline acetyltransferase-positive motor neurons in the lumbar spinal cord. These findings suggest that matrine promotes remodeling and reconnection of neural circuits to regulate hindlimb movement. All protocols were approved by the Committee for Animal Care and Use of the Sugitani Campus of the University of Toyama(approval No. A2013 INM-1 and A2016 INM-3) on May 7, 2013 and May 17, 2016, respectively.

关键词： matrine chronic spinal cord injury axonal growth synaptogenesis hindlimb locomotor presynapse immunohistochemistry Basso Mouse Scale Body Support Score Sophora flavescens

Cathepsins in neuronal plasticity

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Neural Regeneration Research 2021年第1期16卷 26-35页

作者： Amanda Phuong Tran Jerry Silver Center for Integrative Brain Research Seattle Children’s Research InstituteSeattleWAUSA Department of Neurosciences Case Western Reserve UniversityClevelandOHUSA

Proteases comprise a variety of enzymes defined by their ability to catalytically hydrolyze the peptide bonds of other proteins,resulting in protein lysis.Cathepsins,specifically,encompass a class of at least twenty proteases with potent endopeptidase activity.They are located subcellularly in lysosomes,organelles responsible for the cell’s degradative and autophagic processes,and are vital for normal lysosomal function.Although cathepsins are involved in a multitude of cell signaling activities,this chapter will focus on the role of cathepsins(with a special emphasis on Cathepsin B)in neuronal plasticity.We will broadly define what is known about regulation of cathepsins in the central nervous system and compare this with their dysregulation after injury or disease.Importantly,we will delineate what is currently known about the role of cathepsins in axon regeneration and plasticity after spinal cord injury.It is well established that normal cathepsin activity is integral to the function of lysosomes.Without normal lysosomal function,autophagy and other homeostatic cellular processes become dysregulated resulting in axon dystrophy.Furthermore,controlled activation of cathepsins at specialized neuronal structures such as axonal growth cones and dendritic spines have been positively implicated in their plasticity.This chapter will end with a perspective on the consequences of cathepsin dysregulation versus controlled,localized regulation to clarify how cathepsins can contribute to both neuronal plasticity and neurodegeneration.

关键词： axon regeneration cathepsin CSPGs extracellular matrix growth cone lysosomes neuronal plasticity protease remodeling spinal cord injury synaptogenesis