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神经损伤与功能重建 2023年第5期18卷 F0003-F0003页

作者： Mandy S J Kater Katharina F Baumgart Aina Badia-Soteras Tim S Heistek Karen E Carney A Jacob Timmerman Jan R T vanWeering August B Smit Marjo S van der Knaap Huibert D Mansvelder Mark H G Verheijen Rogier Min Department of Molecular and Cellular neurobiology Center for Neurogenomics and Cognitive ResearchAmsterdam NeuroscienceVrije Universiteit AmsterdamThe Netherlands Department of Child Neurology Amsterdam Leukodystrophy CenterEmma Children's HospitalAmsterdam University Medical CentersAmsterdam NeuroscienceAmsterdamThe Netherlands Department of Integrative Neurophysiology Center for Neurogenomics and Cognitive ResearchAmsterdam NeuroscienceVrije Universiteit AmsterdamAmsterdamThe Netherlands Department of Human Genetics Center for Neurogenomics and Cognitive ResearchAmsterdam University Medical CentersAmsterdam NeuroscienceVrije Universiteit AmsterdamAmsterdamThe Netherlands

星形胶质细胞膜蛋白MLC1的功能丧失是伴皮质下囊肿的巨脑性白质脑病(MLC)的主要遗传原因,这一罕见病的特征是脑内离子和水稳态失衡。MLC1蛋白主要分布于大脑中的液体屏障周围,例如在星形胶质细胞接触血管的终足和接触脑膜的突起中。该... 详细信息

星形胶质细胞膜蛋白MLC1的功能丧失是伴皮质下囊肿的巨脑性白质脑病(MLC)的主要遗传原因,这一罕见病的特征是脑内离子和水稳态失衡。MLC1蛋白主要分布于大脑中的液体屏障周围,例如在星形胶质细胞接触血管的终足和接触脑膜的突起中。该蛋白是否在其他星形胶质细胞结构域中发挥作用尚不清楚。本研究表明MLC1存在于星形胶质细胞远端突起中,也称为突触周围星形胶质细胞突起(PAP)或星形胶质细胞小叶;在海马CA1区域它们与兴奋性突触密切相互作用。我们发现在Mlc1缺失小鼠中,向兴奋性突触延伸的PAP末端缩短。这一改变会影响谷氨酸能突触传递,导致自发释放事件的速率降低,并在具有挑战性的条件下减慢谷氨酸的再摄取。此外,虽然野生型小鼠中的PAP在恐惧调节过程从突触回缩,但我们发现在Mlc1缺失小鼠中,这种结构可塑性在本已更短的PAP出现障碍。最后,Mlc1缺失小鼠显示情境恐惧记忆减少。总之,本研究揭示了星形胶质细胞蛋白MLC1在调节PAP结构方面的意想不到的作用。MLC1的缺失会改变兴奋性突触传递,阻止恐惧调节诱导的正常PAP重塑,并破坏情境恐惧记忆表达。因此,MLC1是调节星形胶质细胞-突触相互作用的新参与者。

关键词： MLC1 星形胶质细胞恐惧调节突触周围星形胶质细胞突起突触传递

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小胶质细胞控制成年小鼠海马中的谷氨酸能突触

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神经损伤与功能重建 2021年第10期16卷 F0003-F0003页

作者： Bernadette Basilico Laura Ferrucci Patrizia Ratano Maria T Golia Alfonso Grimaldi Maria Rosito Valentina Ferretti Ingrid Reverte Caterina Sanchini Maria C Marrone Maria Giubettini Valeria De Turris Debora Salerno Stefano Garofalo Marie-Kim St-Pierre Micael Carrier Massimiliano Renzi Francesca Pagani Brijesh Modi Marcello Raspa Ferdinando Scavizzi Cornelius T Gross Silvia Marinelli Marie-Ève Tremblay Daniele Caprioli Laura Maggi Cristina Limatola Silvia Di Angelantonio Davide Ragozzino Department of Physiology and Pharmacology Sapienza University of RomeRomeItaly. Neurophysiology and Neuropharmacology Inflammaging Unit IRCCS NeuromedMediterranean Neurological InstitutePozzilliISItaly. Center for Life Nano-and Neuro-science Istituto Italiano di TecnologiaRomeItaly. Dipartimento di Biologia e Biotecnologie“Charles Darwin” Sapienza University of RomeRomeItaly. Santa Lucia Foundation(IRCCS Fondazione Santa Lucia) RomeItaly. European Brain Research Institute(EBRI)‘Rita Levi-Montalcini’ RomeItaly. CrestOptics S.p.A RomeItaly. Centre de Recherche du CHU de Québec Axe Neurosciences QuébecQuebec CityCanada. Département de Médecine Moléculaire UniversitéLaval QuébecQuebec CityCanada.1 National Research Council Institute of Biochemistry and Cell Biology(CNR-IBBC/EMMA/Infrafrontier/IMPC)International Campus“A.Buzzati-Traverso”Monterotondo(Rome)Italy.1 Epigenetics and neurobiology Unit European Molecular Biology Laboratory(EMBL)MonterotondoItaly.1 Division of Medical Sciences University of VictoriaVictoriaCanada.1 Department of Physiology and Pharmacology Sapienza UniversityLaboratory affiliated to Istituto Pasteur ItaliaRomeItaly.

小胶质细胞是调节大脑突触发育和可塑性的重要细胞类型,但其影响突触的正常功能的机制尚不清楚。在本研究中,我们通过PLX5622造成小胶质细胞耗竭,并观察其对成年野生型小鼠海马CA3-CA1突触的影响。在小胶质细胞耗竭后,与树突棘密度降低... 详细信息

小胶质细胞是调节大脑突触发育和可塑性的重要细胞类型,但其影响突触的正常功能的机制尚不清楚。在本研究中,我们通过PLX5622造成小胶质细胞耗竭,并观察其对成年野生型小鼠海马CA3-CA1突触的影响。在小胶质细胞耗竭后,与树突棘密度降低相关的自发和诱发谷氨酸能活动的减少,出现未成熟突触特征以及突触的可塑性提高。小胶质细胞耗竭的小鼠在新物体识别任务的获取方面表现出缺陷。海马星形胶质细胞出现增生,但并没有神经炎症反应。在Cx3cr1-/-小鼠中,PLX不能导致海马出现上述改变。这说明CX3CL1/CX3CR1轴在小胶质细胞对突触功能的控制中有重要作用。PLX5622停用后,小胶质细胞的重新增殖,海马突触恢复,小鼠的学习功能也出现恢复。综上所述,小胶质细胞对维持成人大脑的突触的正常功能用重要的作用,去除小胶质细胞会导致谷氨酸能突触组织和活动的可逆变化。

关键词：谷氨酸能传递海马体学习小胶质细胞神经元-小胶质细胞相互作用突触

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Iatrogenic opioid dependence is endemic and legal: Genetic addiction risk score (GARS) with electrotherapy a paradigm shift in pain treatment programs

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Health 2013年第11期5卷 16-34页

作者： Kenneth Blum David Han Marlene Oscar-Berman Gary Reinl Nicholas DiNubile Margaret A. Madigan Anish Bajaj Bernard William Downs John Giordano Wayne Westcott Leonard Smith Eric R. Braverman Kristina Dushaj Mary Hauser Thomas Simpatico Thomas McLaughlin Joan Borsten Debmayla Barh Center for Psychiatric Medicine North Andover USA Centre for Genomics and Applied Gene Technology Institute of Integrative Omics and Applied Biotechnology (IIOAB) Nonakuri Purba Medinipur India Department of Addiction Research & Therapy Malibu Beach Recovery Center Malibu Beach USA Department of Executive Health Path Research Foundation NY New York USA Department of Exercise Science Quincy College Quincy USA Department of Holistic Medicine and Pain Track National Institute for Holistic Addiction Studies North Miami Beach USA Department of Management Science and Statistics The University of Texas at San Antonio San Antonio USA Department of Molecular Nutrition Impact Genomics Inc. Austin USA Igene LLC Austin USA Department of Psychiatry Anatomy & Neurobiology Boston VA and Boston University School of Medicine Boston USA Department of Psychiatry College of Medicine & McKnight Brain Institute University of Florida Gainesville USA Department of Executive Health Path Research Foundation NY New York USA Department of Psychiatry College of Medicine & McKnight Brain Institute University of Florida Gainesville USA Electronic Waveform Lab Department of Pain Research Huntington Beach USA Department of Orthopedic Surgery Hospital of the University of Pennsylvania Philadelphia USA Department of Molecular Nutrition Impact Genomics Inc. Austin USA Department of Executive Health Path Research Foundation NY New York USA Department of Holistic Medicine and Pain Track National Institute for Holistic Addiction Studies North Miami Beach USA Dominion Diagnostics LLC North Kingstown USA Department of Psychiatry Human Integrated Services Unit of Vermont Center for Clinical & Translational Science University of Vermont College of Medicine Burlington USA Department of Addiction Research & Therapy Malibu Beach Recovery Center Malibu Beach USA Centre for Genomics and Applied Gene Technology Institute of Integrative Omics and Applied Biotechnology (IIOAB) Nonakuri Purba Me

The mounting endemic of prescription iatrogenic opioid dependence in pain patients provoked this treatise about an alternative method that can be used to treat pain, improve function and reduce the risk of opioid dependence. It is well known that as well as the side effects reported for chronic opioid therapy, genetically predisposed individuals are at risk for opioid dependence. We propose the use of the Genetic Addiction Risk Score (GARS) assessment to identify patients early in treatment who should avoid narcotic pain medications. Primarily, this review will be an exploration of the mechanisms of action of an electrotherapeutic alternative to narcotic treatment that can be used to augment tissue healing and reduce the pain associated with human injuries and neuropathies. This particular electrotherapeutic device was developed at the Electronic Waveform laboratory in Huntington Beach, California and is called the H-Wave? device. The primary effect of the H-Wave?device is stimulation (HWDS) of small diameter fibers of “red-slow-twitch” skeletal muscle. Mechanisms of action of HWDS have been investigated in both animal and human studies. They include edema reduction, induction of nitric oxide dependent augmented microcirculation and angiogenesis, small muscle contraction that eliminates transcapillary fluid shifts, reducing the painful effects of tetanizing fatigue and gradual loading of healing injured muscle tissue that helps repair and remodeling. A recent metaanalysis found a moderate-to-strong-positive effect of the HWDS in providing pain relief, reducing the requirement for pain medication, with the most robust effect being increased functionality. We are proposing that GARS can be used to identify those at risk of developing opioid dependence and that the need for opioid analgesia can be reduced by use of this electro therapeutic alternative to opioid analgesia in the treatment of pain and injuries.

关键词： Microcirculation Angiogenesis Analgesic Therapy Electrical Device Stimulation Tissue Loading Remodeling Genetic Addiction Risk Score (GARS) Reward Deficiency Syndrome (RDS)

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弓形虫感染引起小胶质细胞与神经元的接触以及细胞体周边抑制性突触丧失

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神经损伤与功能重建 2020年第3期15卷 F0004-F0004页

作者： Carrillo GL Ballard VA Glausen T Boone Z Teamer J Hinkson CL Wohlfert EA Blader IJ Fox MA 杜一星(编译) Center for neurobiology Research Fralin Biomedical Research Institute at Virginia Tech CarilionRoanokeVirginiaUSA Graduate Program in Translational Biology Medicineand HealthVirginia TechBlacksburgVirginiaUSA Roanoke Valley Governor's School RoanokeVirginiaUSA Department of Microbiology and Immunology University at BuffaloBuffaloNew YorkUSA School of Neuroscience Virginia TechBlacksburgVirginiaUSA FBRI neuroSURF Program RoanokeVirginiaUSA Virginia Tech Carilion School of Medicine RoanokeVirginiaUSA Department of Biological Sciences Virginia TechBlacksburgVirginiaUSA Department of Pediatrics Virginia Tech Carilion School of MedicineRoanokeVirginiaUSA 不详

大脑内的感染和炎症会引起神经元连通性和功能的改变。细胞内的原生动物寄生虫,弓形虫,是一种感染脑部的病原体,可引起脑炎和癫痫发作。这种寄生虫的持续感染还与行为改变和发生精神疾病(包括精神分裂症)的风险增加有关。目前来自人类... 详细信息

大脑内的感染和炎症会引起神经元连通性和功能的改变。细胞内的原生动物寄生虫,弓形虫,是一种感染脑部的病原体,可引起脑炎和癫痫发作。这种寄生虫的持续感染还与行为改变和发生精神疾病(包括精神分裂症)的风险增加有关。目前来自人类和小鼠模型的研究证据表明,癫痫发作和精神分裂症均由抑制性突触的丧失或功能障碍引起。与此相符,我们最近报道了持续性弓形虫感染改变谷氨酸脱羧酶67(GAD67)的分布,该酶在抑制性突触中催化GABA的合成。这些变化可能反映突触前装置在抑制性神经元中的重新分布或抑制性神经末梢的丧失。为了直接评估后者的可能性,我们采用序列块面扫描电子显微镜(SBFSEM)并量化寄生虫感染后新皮质和海马中的细胞体周边抑制性突触。持续感染不仅导致明显的细胞体周边突触丧失,而且还诱导髓样来源的细胞对神经元细胞体的包封。免疫组织化学、遗传和超微结构分析显示,这些髓样来源的细胞包括活化的小胶质细胞。最后,超微结构分析确定了包膜于细胞体周围神经末梢的髓样来源的细胞,提示它们可能会主动置换或吞噬突触元件。因此,这些结果表明,活化的小胶质细胞有助于寄生虫感染后细胞体周围抑制突触损失,并对于弓形虫的持续感染可能如何导致癫痫发作和精神疾病提供了一种新的机制。

关键词：弓形虫海马抑制性突触小胶质细胞新皮质细胞体周边突触

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Correction:Clinical outcome measures in dementia with Lewy bodies trials:critique and recommendations

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Translational Neurodegeneration 2022年第1期11卷 588-588页

作者： Federico Rodriguez-Porcel Kathryn A.Wyman-Chick Carla Abdelnour Ruiz Jon B.Toledo Daniel Ferreira Prabitha Urwyler Rimona S.Weil Joseph Kane Andrea Pilotto Arvid Rongve Bradley Boeve John-Paul Taylor Ian McKeith Dag Aarsland Simon J.G.Lewis the Lewy Body Dementias Clinical Trials Workgroup from the Lewy Body Dementias Professional Interest Area-Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment(ISTAART) Department of Neurology Medical University of South Carolina208b Rutledge Av.CharlestonSC 29403USA Department of Neurology Center for Memory and AgingHealthPartnersSaint PaulMNUSA Autonomous University of Barcelona BarcelonaSpain Fixel Institute for Neurological Diseases University of FloridaGainesvilleFLUSA Division of Clinical Geriatrics Department of NeurobiologyCare Sciencesand SocietyCenter for Alzheimer’s ResearchKarolinska InstitutetStockholmSweden Department of Radiology Mayo ClinicRochesterMNUSA ARTORG Center for Biomedical Engineering Research University of BernBernSwitzerland Dementia Research Centre University College LondonLondonUK Centre for Public Health Queen’s UniversityBelfastUK Neurology Unit Department of Clinical and Experimental SciencesUniversity of BresciaBresciaItaly Department of Research and Innovation Helse FonnaHaugesund HospitalHaugesundNorway Institute of Clinical Medicine(K1) The University of Ber-genBergenNorway Department of Neurology Center for Sleep MedicineMayo ClinicRochesterMNUSA Translational and Clinical Research Institute Newcastle University Newcastle upon TyneUK Department of Old Age Psychiatry Institute of Psychiatry Psychology and Neuroscience King’s College LondonLondonUK ForeFront Parkinson’s Disease Research Clinic Brain and Mind CentreSchool of Medical SciencesUniversity of Sydney100 Mallett StreetCamperdownNSW 2050Australia. 不详

Correction to:Translational Neurodegeneration(2022)11:24 https://***/10.1186/s40035-022-00299-w Following publication of the original article[1],the authors identified some errors in the Additional files *** original ... 详细信息

关键词： degeneration Clinical measures

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