J.Neurosci.：神经胶质细胞异常导致意识障碍―生命经纬新闻中心

当前位置：生命经纬>新闻中心>神经生物学>文章正文J.Neurosci.：神经胶质细胞异常导致意识障碍来源：生物谷|2009-7-9|阅读次

近日，日本自然科学研究机构生理学研究所的一个研究小组实验证实，精神分裂症主要症状之一的意识障碍是一种被称为神经胶质的细胞出现构造异常所引起的，这种细胞包围着神经细胞。据介绍，日本研究人员首先培育出一种实验大鼠，并特意让这种大鼠神经胶质细胞中的一个基因出现异常，然后观察电流信号在大鼠神经细胞之间传输的过程中其速度的变化情况。结果发现，电流信号的传输速度只有正常大鼠的一半。研究人员用电子显微镜观察发现，出现这种现象的原因就是神经胶质细胞的构造出现了细微的异常变化，即本该完全包住神经细胞突起的神经胶质细胞的顶端并没有完全闭合，从而使神经细胞突起露出了一部分，这也正是导致患者出现意识障碍的原因。一直以来，人们都以为是神经细胞本身出了问题才导致意识障碍，没想到真正的原因竟是神经胶质细胞出现的细微变化，这一结果就连研究人员也连呼意外。精神分裂症是一种具有代表性的精神病，有不少人受这种疾病困扰。精神分裂症又分为阳性症状（妄想和幻觉）、阴性症状（情感障碍，缺乏社交性）和此次研究所涉及的意识障碍（意志活动低下）三大类。（生物谷Bioon.com）生物谷推荐原始出处：TheJournalofNeuroscience,July1,2009,doi:10.1523/JNEUROSCI.3216-08.2009MicewithAlteredMyelinProteolipidProteinGeneExpressionDisplayCognitiveDeficitsAccompaniedbyAbnormalNeuronCGliaInteractionsandDecreasedConductionVelocitiesHisatakaTanaka,1*JianmeiMa,1,5*KenjiF.Tanaka,1*KeizoTakao,6,7MunekazuKomada,2,10KoichiTanda,6AyakaSuzuki,8TomokoIshibashi,8HirokoBaba,8TadashiIsa,3RyuichiShigemoto,4KatsuhikoOno,9TsuyoshiMiyakawa,2,6,7,10andKazuhiroIkenaka1,101DivisionofNeurobiologyandBioinformatics,2CenterforGeneticAnalysisofBehavior,3DepartmentofDevelopmentalPhysiology,and4DivisionofCerebralStructure,NationalInstituteforPhysiologicalSciences,NationalInstitutesofNaturalSciences,Okazaki,Aichi444-8787,Japan,5DepartmentofAnatomy,DalianMedicalUniversity,Dalian,Liaoning116044,China,6GeneticEngineeringandFunctionalGenomicsGroup,HorizontalMedicalResearchOrganization,KyotoUniversityFacultyofMedicine,Sakyo-ku,Kyoto606-8501,Japan,7DivisionofSystemsMedicine,InstituteforComprehensiveMedicalScience,FujitaHealthUniversity,Aichi470-1192,Japan,8DepartmentofMolecularNeurobiology,SchoolofPharmacy,TokyoUniversityofPharmacyandLifeSciences,Hachioji192-0392,Japan,9DepartmentofBiology,KyotoPrefecturalUniversityofMedicine,Kyoto602-8566,Japan,and10JapanScienceandTechnologyAgency,CoreResearchforEvolutionaryScienceandTechnology,Kawaguchi332-0012,JapanConductionvelocity（CV）ofmyelinatedaxonshasbeenshowntoberegulatedbyoligodendrocytesevenaftermyelinationhasbeencompleted.However,howmyelinatingoligodendrocytesregulateCV,andwhatthesignificanceofthisregulationisfornormalbrainfunctionremainunknown.Toaddressthesequestions,weanalyzedatransgenicmouselineharboringextracopiesofthemyelinproteolipidprotein1（plp1）gene（plp1tg/Cmice）at2monthsofage.Atthisstage,theplp1tg/Cmicehaveanunaffectedmyelinstructurewithanormallyappearingionchanneldistribution,buttheCVinallaxonaltractstestedintheCNSisgreatlyreduced.Wealsofounddecreasedaxonaldiametersandslightlyabnormalparanodalstructures,bothofwhichcanbeacauseforthereducedCV.Interestinglytheplp1tg/Cmiceshowedalteredanxiety-likebehaviors,reducedprepulseinhibitions,spatiallearningdeficitsandworkingmemorydeficit,allofwhichareschizophrenia-relatedbehaviors.Ourresultsimplicatethatabnormalitiesintheneuron-gliainteractionsattheparanodaljunctionscanresultinreducedCVintheCNS,whichtheninducesbehavioralabnormalitiesrelatedtoschizophrenia.