简介：

简介：Thehippocampalregionofthebrainisimportantforencodingenvironmentinputsandmemoryformation.However,theunderlyingmechanismsareunclear.ToinvestigatethebehaviorofindividualneuronsinresponsetosomatosensoryinputsinthehippocampalCA1region,werecordedandanalyzedchangesinlocalfieldpotentialsandthefiringratesofindividualpyramidalcellsandinterneuronsduringtailclampinginurethane-anesthetizedrats.Wealsoexploredthemechanismsunderlyingtheneuronalresponses.Somatosensorystimulation,intheformoftailclamping,changedlocalfieldpotentialsintothetarhythm-dominatedwaveforms,decreasedthespikefiringofpyramidalcells,andincreasedinterneuronfiring.Inaddition,somatosensorystimulationattenuatedorthodromic-evokedpopulationspikes.TheseresultssuggestthatsomatosensorystimulationsuppressestheexcitabilityofpyramidalcellsinthehippocampalCA1region.Increasedinhibitionbylocalinterneuronsmightunderliethiseffect.Thesefindingsprovideinsightintothemechanismsofsignalprocessinginthehippocampusandsuggestthatsensorystimulationmighthavetherapeuticpotentialforbraindisordersassociatedwithneuronalhyperexcitability.

简介：Theactiveingredientofginseng,ginsenosidesRg1,hasbeenshowntoscavengefreeradicalsandimproveantioxidantcapacity.ThisstudyhypothesizedthatginsenosidesRg1hasaprotectiveroleinhumanneuroblastomacellsinjuredbyH_2O_2.GinsenosidesRg1atdifferentconcentrations(50and100μM)wasusedtotreatH_2O_2(150μM)-injuredSH-SY5Ycells.ResultsdemonstratedthatginsenosideRg1elevatedthesurvivalrateofSH-SY5YcellsinjuredbyH_2O_2,diminishedtheamountofleakedlactatedehydrogenase,andincreasedsuperoxidedismutaseactivity.GinsenosideRg1effectivelysuppressedcaspase-3immunoreactivity,andcontributedtoheatshockprotein70geneexpression,inadose-dependentmanner.TheseresultsindicatethatginsenosideRg1hasprotectiveeffectsonSH-SY5YcellsinjuredbyH_2O_2andthatitsmechanismofactionisassociatedwithanti-oxidationandtheinhibitionofapoptosis.

简介：Parthenogeneticembryonicstemcellshavepluripotentdifferentiationpotentials,akintofertilizedembryo-derivedembryonicstemcells.Theaimofthisstudywastocomparetheneuronaldifferentiationpotentialofparthenogeneticandfertilizedembryo-derivedembryonicstemcells.Beforedifferentiation,karyotypeanalysiswasperformed,withnormalkaryotypesdetectedinbothparthenogeneticandfertilizedembryo-derivedembryonicstemcells.SexchromosomeswereidentifiedasXX.Immunocytochemistryandquantitativereal-timePCRdetectedhighexpressionofthepluripotentgene,Oct4,atboththemRNAandproteinlevels,indicatingpluripotentdifferentiationpotentialofthetwoembryonicstemcellsubtypes.Embryonicstemcellswereinducedwithretinoicacidtoformembryoidbodies,andthendispersedintosinglecells.SinglecellsweredifferentiatedinN2differentiationmediumfor9days.Immunocytochemistryshowedparthenogeneticandfertilizedembryo-derivedembryonicstemcellsbothexpresstheneuronalcellmarkersnestin,βIII-tubulinandmyelinbasicprotein.Quantitativereal-timePCRfoundexpressionofneurogenesisrelatedgenes(Sox-1,Nestin,GABA,Pax6,Zic5andPitx1)inbothtypesofembryonicstemcells,andOct4expressionwassignificantlydecreased.NestinandPax6expressioninparthenogeneticembryonicstemcellswassignificantlyhigherthanthatinfertilizedembryo-derivedembryonicstemcells.Thus,ourexperimentalfindingsindicatethatparthenogeneticembryonicstemcellshavestrongerneuronaldifferentiationpotentialthanfertilizedembryo-derivedembryonicstemcells.

简介：BACKGROUND:Duetothelackofautografttransplantrejection,Schwanncells(SCs)canpromotetheproliferationofembryonicstemcellsandtheinductionofdopaminergicneurons.Mesencephalicstemcellscanbeinducedtoproducedopaminergicneurons.Thetherapeuticeffectsofco-graftsofSCsandneuralstemcells(NSCs)deservesfurtherstudyandverificationinParkinsoniananimalmodels.OBJECTIVE:ToinvestigatetheeffectsofSchwanncellsandmesencephalicNSCco-graftsinParkinsoniananimalmodelsonanimalbehaviorandhistology.DESIGN:Randomizedcontrolledexperiment.SETTING:FudanUniversity;InstituteofNeuroscience,ChineseAcademyofSciences.MATERIALS:ThefollowinganimalswereobtainedfromtheExperimentalAnimalCenter,ShanghaiInstituteforBiologicalScience,ChineseAcademyofSciences:5Sprague-Dawleyrats,embryonicday(E)13-16;16neonatalSprague-Dawleyrats,postnatalday1-3;and18adultSDratsofbothgenders.Animalexperimentationmetanimalethicalapproval.METHODS:TheexperimentwasperformedattheDepartmentofAnatomy,HistologyandEmbryology,ShanghaiMedicalCenter,FudanUniversityfromSeptember2005toJanuary2007.ThemesencephalicNSCswereobtainedfromthebrainsofSDratsatE13-16,andSCswereharvestedfromthesciaticnervesofneonatalratsatday1-3.Hemiparkinsonianrats(n=18)wereselectedfortransplantationafterestimatingrotationalbehaviorinresponsetoapomorphineandwererandomlyassignedtothreegroups:controlgroup,NSCgroup,andco-graftgroup.Therewere6ratsineachgroup.Eitherphosphatebufferedsaline(PBS),NSCs,orSCsplusNSCsweretransplantedintotherightneostriatumofParkinsonianrats,respectively.MAINOUTCOMEMEASURES:①Rotationalbehaviorwasinducedbyapomorphine(0.05mg/kg,i.p.)2,4,6,8,and10weeksaftertransplantation,andthenumberofrotationswerecounted.②Differentiationandsurvivalofdopaminergicneuronsintherightneostriatumwerequantifiedbytyrosinehydroxylaseimmu

简介：MicroRNAs(miRNAs)aresmall,non-codingRNAsthatnegativelyadjustgeneexpressioninmultifariousbiologicalprocesses.However,theregulatoryeffectsofmiRNAsonSchwanncellsremainpoorlyunderstood.PreviousmicroarrayanalysisresultshaveshownthatmiRNAexpressionisalteredfollowingsciaticnervetransaction,therebyaffectingproliferationandmigrationofSchwanncells.ThisstudyinvestigatedwhethermiR-148b-3pcouldregulatemigrationofSchwanncellsbydirectlytargetingcullin-associatedandneddylation-dissociated1(Cand1).Up-regulatedexpressionofmiR-148b-3ppromotedSchwanncellmigration,whereassilencingofmiR-148b-3pinhibitedSchwanncellmigrationinvitro.FurtherexperimentsconfirmedthatCandlwasadirecttargetofmiR-148b-3p,andCandlknockdownreversedsuppressionofthemiR-148b-3pinhibitoronSchwanncellmigration.TheseresultssuggestedthatmiR-148b-3ppromotedmigrationofSchwanncellsbydirectlytargetingCandlinvitro.

简介：Intracerebralhemorrhage(ICH)isthemostseverecerebrovasculardisease,whichrepresentsaleadingcauseofdeathanddisabilityindevelopedcountries.However,therapeuticoptionsarelimited,soismandatorytoinvestigaterepairingprocessesafterstrokeinordertodevelopnewtherapeuticstrategiesabletopromotebrainrepairprocesses.TherapeuticangiogenesisandvasculogenesisholdpromisetoimproveoutcomeofICHpatients.Inthisregard,circulatingendothelialprogenitorcells(EPCs)haverecentlybeensuggestedtobeamarkerofvascularriskandendothelialfunction.Moreover,EPClevelshavebeenassociatedwithgoodneurologicalandfunctionaloutcomeaswellasreducedresidualhematomavolumeinICHpatients.Finally,experimentalandclinicalstudiesindicatethatEPCmightmediateendothelialcellregenerationandneovascularization.Therefore,EPC-basedtherapycouldbeanexcellenttherapeuticoptioninICH.Inthismini-review,wediscussthepresentstatusofknowledgeaboutthepossibletherapeuticroleofEPCsinICH,molecularmechanisms,andthefutureperspectivesandstrategiesfortheiruseinclinicalpractice.

简介：Withinthenervoussystem,regenerationislimited,andthisisduetothesmallamountofneuralstemcells,theinhibitoryoriginofthestemcellnicheandoftentothedevelopmentofascarwhichconstitutesamechanicalbarrierfortheregeneration.Regardingtheseaspects,manyeffortshavebeendoneintheresearchofacellcomponentthatcombinedwithscaffoldsandgrowthfactorscouldbesuitablefornervousregenerationinregenerativemedicineapproaches.Autologousmesenchymalstemcellsrepresentnowadaystheidealcandidateforthisaim,thanktotheirmultipotencyandtotheiramountinsideadulttissues.However,issuesintheirharvesting,throughtheuseofinvasivetechniques,andproblemsinvolvedintheirageing,requiretheresearchofnewautologoussources.Tothispurpose,therecentdiscoveryofastemcellscomponentinteeth,andwhichderivefromneuralcrestcells,hascametothelightthepossibilityofusingdentalstemcellsinnervoussystemregeneration.Inthiswork,inordertogiveguidelinesontheuseofdentalstemcellsforneuralregeneration,webrieflyintroducetheconceptsofregenerationandregenerativemedicine,wethenfocustheattentiononodontogenesis,whichinvolvestheformationandthepresenceofastemcomponentindifferentpartsofteeth,andfinallywedescribesomeexperimentalapproacheswhichareexploitingdentalstemcellsforneuralstudies.

简介：1-methyl-4-phenylpyridiniumion(MPP+)inducesendoplasmicreticulumstressandactivatescaspase-12inPC12cells,leadingtoneuronalapoptosis.However,theunderlyingmolecularmechanismremainsunknown.Thepresentstudyinvestigatedtheregulatoryeffectsofnervegrowthfactor(Aktactivator)andlithiumchloride(glycogensynthasekinase-3βinhibitor)ontheendoplasmicreticulumstresssignalingpathway.TheresultsrevealedthatMPP+inducedexpressionofBipandC/EBPhomologousprotein.TheupregulationofBipandC/EBPhomologousprotein,aswellasthedecreasedpro-caspase-12levelinducedbyMPP+wereinhibitedbypretreatmentofthenervegrowthfactororlithiumchloride.Theseresultssuggestthatthephosphatidylinositol3kinase-Akt-glycogensynthasekinase-3βpathwayisinvolvedinMPP+-inducedendoplasmicreticulumstress.

简介：Asingeniousasnature'sinventionofmyelinsheathswithinthemammaliannervoussystemis,asfatalcanbedamagetothisspecializedlipidstructure.Long-termlossofelectricalinsulationandoffurthersupportivefunctionsmyelinprovidestoaxons,asseenindemyelinatingdiseasessuchasmultiplesclerosis(MS),leadstoneurodegenerationandresultsinprogressivedisabilities.Multiplelinesofevidencehavedemonstratedtheincreasinginabilityofoligodendrocyteprecursorcells(OPCs)toreplacelostoligodendrocytes(OLs)inordertorestorelostmyelin.Muchresearchhasbeendedicatedtorevealpotentialreasonsforthisregenerationdeficitbutdespitepromisingapproachesnoremyelination-promotingdrugshavesuccessfullybeendevelopedyet.InadditiontoOPCsneuralstemcellsoftheadultcentralnervoussystemalsoholdahighpotentialtogeneratemyelinatingOLs.Thereareatleasttwoneuralstemcellnichesinthebrain,thesubventricularzoneliningthelateralventriclesandthesubgranularzoneofthedentategyrus,andanadditionalsourceofneuralstemcellshasbeenlocatedinthecentralcanalofthespinalcord.Whileasubstantialbodyofliteraturehasdescribedtheirneurogeniccapacity,stilllittleisknownabouttheoligodendrogenicpotentialofthesecells,evenifsomeanimalstudieshaveprovidedproofoftheircontributiontoremyelination.Inthisreview,wesummarizeanddiscussthesestudies,takingintoaccountthedifferentniches,theheterogeneitywithinandbetweenstemcellnichesandpresentcurrentstrategiesofhowtopromotestemcell-mediatedmyelinrepair.

简介：BACKGROUND:Gliomaisthemostcommonintracranialtumorandhasapoorpatientprognosis.Thepresenceofbraintumorstemcellswasgraduallybeingunderstoodandrecognized,whichmightbebeneficialforthetreatmentofglioma.OBJECTIVE:Tousebibliometricindexestotrackstudyfocusesongliomastemcell,andtoinvestigatetherelationshipsamonggeographicorigin,impactfactors,andhighlycitedarticlesindexedinWebofScience.METHODS:AlistofcitationclassicsforgliomastemcellswasgeneratedbysearchingthedatabaseofWebofScience-Expandedusingtheterms"gliomastemcell"or"glioma,stemcell’"or"braintumorstemcell".Thetop63citedresearcharticleswhichwerecitedmorethan100timeswereretrievedbyreadingtheabstractorfulltextifneeded.Eacheligiblearticlewasreviewedforbasicinformationonsubjectcategories,countryoforigin,journals,authors,andsourceofjournals.Inclusivecriteria:(1)articlesinthefieldofgliomastemcellswhichwascitedmorethan100times;(2)fundamentalresearchonhumansoranimals,clinicaltrialsandcasereports;(3)researcharticle;(4)yearofpublication:1899-2012;and(5)citationdatabase:ScienceCitationIndex-Expanded.Exclusivecriteria:(1)articlesneedingtobemanuallysearchedoraccessedonlybytelephone;(2)unpublishedarticles;and(3)reviews,conferenceproceedings,aswellascorrectedpapers.RESULTS:Of2040articlespublished,the63top-citedarticleswerepublishedbetween1992and2010.Thenumberofcitationsrangedfrom100to1754,withameanof280citationsperarticle.Thesecitationclassicscamefromnineteencountries,ofwhich46articlescamefromtheUnitedStates.DukeUniversityandUniversityofCalifornia,SanFranciscoledthelistofclassicswithsevenpaperseach.The63top-citedarticleswerepublishedin28journals,predominantlyCancerResearchandCancerCell,followedbyCellStemCellandNature.CONCLUSION:Ourbibliometricanalysisprovidesahistoricalpersp

简介：Brainmicrovascularendothelialcellsformtheinterfacebetweennervoustissueandcirculatingblood,andregulatecentralnervoussystemhomeostasis.Brainmicrovascularendothelialcellsdifferfromperipheralendothelialcellswithregardsexpressionofspecificiontransportersandreceptors,andcontainfewerfenestrationsandpinocytoticvesicles.Brainmicrovascularendothelialcellsalsosynthesizeseveralfactorsthatinfluencebloodvesselfunction.Thisreviewdescribesthemorphologicalcharacteristicsandfunctionsofbrainmicrovascularendothelialcells,andsummarizescurrentknowledgeregardingchangesinbrainmicrovascularendothelialcellsduringstrokeprogressionandtherapies.Futurestudiesshouldfocusonidentifyingmechanismsunderlyingsuchchangesanddevelopingpossibleneuroprotectivetherapeuticinterventions.

简介：EnhancingSchwanncellproliferationmaybebeneficialforperipheralnerverepairandnerveregeneration.AtraditionalherbalformulacomposedofFuling(poriacocos),Baizhu(Atractylodesmacrocephala),andDanggui(Angelicasinensis)(FBD)improvesneuronalsurvivalandgrowth,andFBDmaypromotethesecretionofbrain-derivedneurotrophicfactor.However,themechanismunderlyingSchwanncellproliferationremainsunclear.WetestedwhetherFBDenhancedtheproliferationofhumanSchwanncells.FBD(20μg/mL)increasedSchwanncellviabilityandsurvival,andincreasedthenumberofcellsatG2/MandSphases.FBDalsoincreasednervegrowthfactorandbrain-derivedneurotrophicfactorexpressioninSchwanncells,withmaximumefficacyat20μg/mL.

简介：BACKGROUND:Alpha-actinin(α-actinin)playsakeyroleinneuronalgrowthconemigrationduringdirectionaldifferentiationfromneuralstemcells(NSCs)toneurons.OBJECTIVE:Todetectinsitumicrodistributionandquantitativeexpressionofα-actininduringdirectionaldifferentiationofNSCstoneuronsinthetemporallobecerebralcortexofneonatalrats.DESIGN,TIMEANDSETTING:BetweenJanuary2006andDecember2008,cultureanddirectionaldifferentiationofNSCswereperformedatDepartmentofHistologyandEmbryology,PreclinicalMedicalCollege,ChinaMedicalUniversity.ImmuneelectronmicroscopywasperformedatDepartmentofHistologyandEmbryologyandDepartmentofElectronMicrology,PreclinicalMedicalCollege,ChinaMedicalUniversity.SpectrumanalysiswasperformedatLaboratoryofElectronMicroscopy,MentalResearchInstitute,ChineseAcademyofSciences.MATERIALS:Basicfibroblastgrowthfactor,epidermalgrowthfactor,brain-derivednervegrowthfactor,type-1insulinlikegrowthfactor,andα-actininantibodywereprovidedbyGibcoBRL,USA;rabbit-anti-ratnestinmonoclonalantibody,rabbit-anti-ratneuronspecificenolasepolyclonalantibody,andEDAX-9100energydispersiveX-rayanalysiswereprovidedbyPHILIPSCompany,Netherlands.METHODS:NSCs,followingprimaryandpassageculture,weredifferentiatedwithserumculturemedium(DMEM/F_(12)+10%fetalbovineserum+2ng/mLbrain-derivednervegrowthfactor+2ng/mLtype-1insulinlikegrowthfactor).MAINOUTCOMEMEASURES:Expressionofα-actinininneuron-likecellswasquantitativelyandqualitativelydetectedwithimmunocytochemistryusingenergydispersiveX-rayanalysis.RESULTS:Immunocytochemistry,combinedwithelectronmicroscopy,indicatedthatpositiveα-actininexpressionwaslikeaspheroidparticlewithhighelectrondensity.Inaddition,theexpressionwasgraduallyconcentratedfromthenuclearedgetothecytoplasmandexpandedintodevelopingneurites,duringdifferentiationofneuralstemcellstoneurons.Conversely,energydispersive

简介：Amyotrophiclateralsclerosis(ALS)isafatalprogressivedisordercharacterizedbytheselectivedegenerationofmotorneurons(MN).TheimpactofperipheralimmunestatusondiseaseprogressionandMNsurvivalisbecomingincreasinglyrecognizedintheALSresearchfield.Inthisreview,webrieflydiscussfindingsfrommousemodelsofperipheralnerveinjuryandimmunodeficiencytounderstandhowtheimmunesystemregulatesMNsurvival.Weextendtheseobservationstosimilarstudiesinthewidelyusedsuperoxidedismutase1(SOD1)mousemodelofALS.Last,wepresentfuturehypothesestoidentifypotentialcausativefactorsthatleadtoimmunedysregulationinALS.Thelessonsfromprecedingworkinthisareaoffernewexcitingdirectionstobridgethegapinourcurrentunderstandingofimmune-mediatedneuroprotectioninALS.

简介：BACKGROUND:Transplantedmononuclearcell(MNC)ofumbilicalbloodcansurviveincentralnervoussystem(CNS)ofhostthroughbloodbrainbarrier,differentiateintonervercells,migratetodamagedsiteandintegratemorphologicalstrucghandfunctionwithnervecellsofhostsoastoimprovedeficienciesofsensatoryfunction,motorfunctionandcognitivefunctionandinfluenceonstrokesequela.OBJECTIVE:Toobservetheveintransplantationofhumanumbilicalcordbloodstemcells(HUCBSC)forimprovingneurologicalfunction,limbfuntionandactivityofdailylivingofpatientswithstrokeandevaluatethereliability.DESIGN:Self-controlledstudy.SETTING:DepartmentofNeurosurgery,theSecondPeople'sHospitalofZhengzhouCity;Red-crossedBloodCenterofHenanProvince;DepartmentofNeurosurgery,theFistAffiliatedHospitalofZhenzhouUniversity.PARTICIPANTS:Atotalof10patientswithstokesequelawereselectedfromDepartmentofCerebralSurgery,theSecondPeople'sHospitalofZhengzhouCityfromApriltoDecember2005.Therewere9malesand1femaleagedfrom35to75yearswiththemeanageof56years.AllofthemwerediagnosedwithCTandMRIexaminationandcoincidencewithdiagnosticcriteriaofstrokeestablishedbytheFourthNationalAcademicMeetingforCerebrovascularDisease.Allpatientsprovidedinformedconsent.METHODS:80-140mLumbilicalbloodoftermbirthofnewbornwasselectedhermeticallyandmaintainedinsterileplasticbag.Andthen,thebloodwascentrifugatedatthespeedof1500r/minfor30minutesat22℃inordertoseparateMNC,i.e.,HUCBSC.Inaddition,afterfinaldiagnosisduringhospitalization,strokepatientswereperfusedwithHUCBSCthroughsuperficialveinofbackofthehand.Eachpatientwasaveragelypenfusedwith6portionsofHUCBSC(cellularnumbers≥1×108/portion)andtheintervalbetweeneachportionwas1-7dayswiththemeanintervalof4days.MAINOUTCOMEMEASURES:①Neurologicalfunctionofstrokepatientswasevaluatedwithneurologicalfunctiondeficiency(NFD)befor

简介：Injurytoaxonsclosetotheneuronalbodiesinthemammaliancentralnervoussystemcausesalargeproportionofparentingneuronstodegenerate.Itisknownthatopticnervetransectionclosetotheeyeinrodentsleadstoalossofabouthalfofretinalganglioncellsin1weekandabout90%in2weeks.Usinglowlevellasertreatmentinthepresentstudy,wedemonstratedthattreatmentwithhelium-neon(660nm)laserwith15mWpowercoulddelayretinalganglioncelldeathafteropticnerveaxotomyinadulthamsters.Theeffectwasmostapparentinthefirstweekwithashortperiodoftreatmenttime(5minutes)inwhich65–66%ofretinalganglioncellssurvivedtheopticnerveaxotomywhereas45–47%ofretinalganglioncellsdidsoinopticnerveaxotomycontrols.Wealsofoundthatsingledoseandearlycommencementoflaserirradiationwereimportantinprotectingretinalganglioncellsfollowingopticnerveaxotomy.Thesefindingsthusconvincinglyshowthatappropriatelasertreatmentmaybeneuroprotectivetoretinalganglioncells.更多还原

简介：ThisstudysoughttoidentifydifferentiallyexpressedproteinsinSH-SY5Ycellstreatedwithvalproicacid,usingtwo-dimensionaldifferencegelelectrophoresisanalysis.Threeproteinswereunambi-guouslyidentified:theeukaryotictranslationinitiationfactor4Aisoform1andATP6V1B2proteinweredownregulated,whiletheheterogeneousnuclearribonucleoproteinKwasupregulated.Moreover,allthreeproteinsareassociatedwithalteredexpressionduetooxidativestress.Ma-trix-assistedlaserdesorption/ionization-timeofflightmassspectrometryandproteinimmunoblottingassayconfirmedthedifferentialexpressionofeukaryotictranslationinitiationfactor4Aisoform1.Theresultsindicatethatvalproicacidexertsanantioxidationeffectbyregulatingtheexpressionofeukaryotictranslationinitiationfactor4Aisoform1.

简介：Membranedepolarizationinducesthereleaseoftheserineproteinasetissue-typeplasminogenactivator(tPA)fromthepresynapticterminalofcerebralcorticalneurons.OnceinthesynapticcleftthistPApromotestheexocytosisandsubsequentendocyticretrievalofglutamate-containingsynapticvesicles,andregulatesthepostsynapticresponsetothepresynapticreleaseofglutamate.Indeed,tPAhasabidirectionaleffectonthecompositionofthepostsynapticdensity(PSD)thatdoesnotrequireplasmingenerationorthepresynapticreleaseofglutamate,butvariesaccordingtothebaselinelevelofneuronalactivity.Hence,ininactiveneuronstPAinducesphosphorylationandaccumulationinthePSDoftheCa~(2+)/calmodulin-dependentproteinkinaseIIα(pCaMKIIα),followedbypCaMKIIα-inducedphosphorylationandsynapticrecruitmentofGluR1-containingα-amino-3-hydroxy-5-methyl-4-isoxazolepropionicacid(AMPA)receptors.Incontrast,inactiveneuronswithincreasedlevelsofpCaMKIIαinthePSDtPAinducespCaMKIIαandpGluR1dephosphorylationandtheirsubsequentremovalfromthePSD.TheseeffectsrequireactivesynapticN-methyl-D-aspartate(NMDA)receptorsandcyclin-dependentkinase5(Cdk5)-inducedphosphorylationoftheproteinphosphatase1(PP1)atT320.ThesedataindicatethattPAisahomeostaticregulatorofthepostsynapticresponseofcerebralcorticalneuronstothepresynapticreleaseofglutamateviabidirectionalregulationofthepCaMKIIα/PP1switchinthePSD.

简介：Similarlytootheradulttissues,ahierarchicalstructurehasbeenestablishedforthebrain,wherethedifferentiatedcelltypes(neurons,oligodendrocytesandastrocytes)aregeneratedfromprimaryprogenitorcells,knownastypeB