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简介：Demyelinationofthecentralnervoussystem(CNS)isahallmarkofmultiplesclerosis(MS),chronicinflammatoryandneurodegenerativedisease.Chronicdemyelinationfavorsneurodegenerationofdenudedaxons,whichisamajorcauseofirreversibleneuronaldeficitsanddisabilityinMSpatients(Lucchinettietal.,2000).MSremainsanincurabledisease,despiteformida-

简介：Multiplesclerosisisachronicinflammatorydiseasethatisaccompaniedbydemyelinationandaxonaldamageresultinginneurologicaldeficits.Remyelinationisthenaturalendogenousrepairmechanismofdemyelinatedaxonsanditissupposedtoprotectaxons/neuronsfromdegenerationandthusthepatientfromprogressivedisability(FranklinandFfrench-Constant,2008).Currenttherapeuticsforpatientswithmultiplesclerosis

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简介：TheRho/Rho-associatedcoiled-coilcontainingproteinkinase(Rho/ROCK)pathwayisamajorsignalingpathwayinthecentralnervoussystem,transducinginhibitorysignalstoblockregeneration.Aftercentralnervoussystemdamage,themaincauseofimpairedregenerationisthepresenceoffactorsthatstronglyinhibitregenerationinthesurroundingmicroenvironment.ThesefactorssignalthroughtheRho/ROCKsignalingpathwaytoinhibitregeneration.Therefore,athoroughunderstandingoftheRho/ROCKsignalingpathwayiscrucialforadvancingstudiesonregenerationandrepairoftheinjuredcentralnervoussystem.

简介：Regenerationinthecentralnervoussystem(CNS)islimited,andCNSdamageoftenleadstocognitiveimpairmentorpermanentfunctionalmotorandsensoryloss.Impairedregenerativecapacityismultifactorialandincludesinflammation,lossofthebloodbrainbarrier,andalterationintheextracellularmatrix(ECM).OneofthemainproblemsistheformationofaglialscarandtheproductionofinhibitoryECM,suchasproteoglycans,that

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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.

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简介：Icariin,themajoractivecomponentofChinesemedicinalherbepimediumbrevicornummaxim,isusedwidelyintraditionalChinesemedicineforthetreatmentofneurologicaldiseases.However,theeffectsoficariinonmyelininhibitoryfactorsareasyetunclear.Inthepresentstudy,administrationoficariinat20mg/kgshowedamarkedreductioninneurologicaldeficitofmiddlecerebralarteryocclusionrats.Icariinexhibitedbetterinhibitoryeffectsonmyelininhibitoryfactors:Nogo-A,myelin-associatedglycoproteinandoligodendrocytemyelinglycoproteininischemiaregionsofmiddlecerebralarteryocclusionratscomparedwithmonosialotetrahexosylganglioside.Theseresultsindicatethaticariinexhibitspotentinhibitoryeffectsonexpressionofmyelininhibitorsaftermiddlecerebralarteryocclusion-inducedfocalcerebralischemiainvivo.Thiseffectmaybemediated,atleastinpart,bytheinhibitionofbothNogo-A,myelin-associatedglycoproteinandoligodendrocytemyelinglycoproteinactivation,followedbytheenhancementofaxonalsproutingandregeneration,resultinginneurologicalfunctionalrecovery.

简介：Mostmigrainepatientssufferfromcutaneousallodynia;however,theunderlyingmechanismsareunclear.Calcitoningene-relatedpeptide(CGRP)playsanimportantroleinthepathophysiologyofmigraine,anditistherefore,apotentialtherapeutictargetfortreatingthepain.Inthepresentstudy,aratmodelofconsciousmigraine,inducedbyrepeatedelectricalstimulationofthesuperiorsagittalsinus,wasestablishedandtreatedwithelectroacupunctureatFengchi(GB20)(depthof2–3mm,frequencyof2/15Hz,intensityof0.5–1.0mA,15minutes/day,for7consecutivedays).ElectroacupunctureatGB20significantlyalleviatedthedecreaseinhindpawandfacialwithdrawalthresholdsandsignificantlylessenedtheincreaseinthelevelsofCGRPinthetrigeminalganglion,trigeminalnucleuscaudalisandventroposteriormedialthalamicnucleusinratswithmigraine.NoCGRP-positivecellsweredetectedinthetrigeminalnucleuscaudalisorventroposteriormedialthalamicnucleusbyimmunofluorescence.Ourfindingssuggestthatelectroacupuncturetreatmentamelioratesmigrainepainandassociatedcutaneousallodyniabymodulatingthetrigeminovascularsystemascendingpathway,atleastinpartbyinhibitingCGRPexpressioninthetrigeminalganglion.

简介：Thestudyaimstoconfirmtheneuroregenerativeeffectsofbacterialmelanin(BM)oncentralnervoussysteminjuryusingaspecialstainingmethodbasedonthedetectionofCa~(2+)-dependentacidphosphataseactivity.Twenty-fourratswererandomlyassignedtoundergoeitherunilateraldestructionofsensorimotorcortex(groupI;n=12)orunilateralrubrospinaltracttransectionatthecervicallevel(C3–4)(groupⅡ;n=12).Ineachgroup,sixratswererandomlyselectedaftersurgerytoundergointramuscularinjectionofBMsolution(BMsubgroup)andtheremainingsixratswereintramuscularlyinjectedwithsaline(salinesubgroup).NeurologicaltestingconfirmedthatBMacceleratedtherecoveryofmotorfunctioninratsfrombothBMandsalinesubgroups.Twomonthsaftersurgery,Ca~(2+)-dependentacidphosphataseactivitydetectionincombinationwithChilingarian'scalciumadenosidetriphosphatemethodrevealedthatBMstimulatedthesproutingoffibersanddilatedthecapillariesinthebrainandspinalcord.TheseresultssuggestthatBMcanpromotetherecoveryofmotorfunctionofratswithcentralnervoussysteminjury;anddetectionofCa~(2+)-dependentacidphosphataseactivityisafastandeasymethodusedtostudytheregeneration-promotingeffectsofBMontheinjuredcentralnervoussystem.