简介:Objective:Toinvestigatetheeffectofmoderatehypothermiaonresponsesofaxonalcytoskeletontoaxonalinjuryintheacutestageofinjury.Methods:Offifteenadultguineapigs,twelveanimalsweresubjectedtostretchinjurytotherightopticnervesanddividedintothenormothermicgroup(n=6)inwhichtheanimal'scoretemperaturewasmaintainedat36.0-37.5℃andthehypothermiagroup(n=6)inwhichthecoretemperaturewasreducedto32.0-32.5℃afterstretchinjury.Remainingthreeanimalssustainednoinjurytotherightopticnervesandservedascontrolgroup.Halfofinjuredanimals(n=3)ofeithernormothermicgrouporhypothermicgroupwerekilledateither2hoursor4hoursafterinjury.Theultrastructuralchangesofaxonalcytoskeletonoftherightopticnervefibersfromtheanimalswereexaminedunderatransmissionelectronmicroscopeandanalyzedbyquantitativeanalysiswithacomputerimageanalysissystem.Results:At2hoursafterstretchinjury,therewasasignificantreductioninthemeannumberofmicrotubules(P<0.001),andasignificantincreaseinthemeanintermicrotubulespacing(P<0.05orP<0.01)inaxonsofallsizesinnormothermicanimals.Themeannumberofneurofilamentsalsodecreasedstatistically(P<0.01)inlargeandmediumsubgroupsofaxonsinthesameexperimentalgroupat2hours.By4hours,thelargesubgroupofaxonsinnormothermicanimalsstilldemonstratedasignificantdeclineinthemeannumberofmicrotubules(P<0.01)andanincreaseinthemeanintermicrotubulespacing(P<0.05),whilethemediumandsmallsubgroupsofaxonsdisplayedasignificantincreaseinthemeannumberofneurofilaments(P<0.05)andreductioninthemeaninterneurofilamentspacing(P<0.05).Onthecontrary,eitherthemeannumberofmicrotubulesandthemeanintermicrotubulespacing,orthemeannumberofneurofilamentsandinterneurofilamentspacinginaxonsofallsizesinhypothermicstretch-injuredanimalswasnotsignificantdifferentfromthemeanvaluesofsham-operated
简介:Diffuseaxonalinjury(DAI)isaxonalandsmallvesselinjuryproducedbyasuddenaccelerationoftheheadbyanexternalforce,andisamajorcauseofdeathandseveredisability(Paterakisetal.,2000).Prognosisispoorerinpatientswithapparenthemorrhagethaninthosewithout(Paterakisetal.,2000).Therefore,itisimportanttoidentifythepresenceandprecisepositionofhemorrhagicfociforamoreaccuratediagnosis.CTandmagneticresonanceimaging(MRI)havelongbeenappliedinthediagnosis
简介:Strokeisaleadingcauseofdeathanddisabilityinadultsworldwide.Fordecades,theprimaryapproachandgoaloftherapyforstrokehasfocusedonneuroprotection,namelytreatingtheinjuredtissue,withinterventionsdesignedtoreducethevolumeofcerebralinfarction.Enormouseffortinthelaboratoryhasbeendevotedtothedevelopmentof
简介:Inthispaper,conditionsfortheexistenceofequilibriumpointsandglobalstabilityareemphaticallydiscussedforBidirectionalAssociativeMemory(BAM)modelswithaxonalsignaltransmissiondelays,andthediscussedmethodsaremoregeneral.Thecorrectnessofobtainedconclusionsisverifiedbyuseofsomeexamples.TheobtainedresultshaveprimarysignificanceinthedesignandapplicationofBAM.
简介:Thedistributionofsensorysymptomsincarpaltunnelsyndromeisstronglydependentonthedegreeofelectrophysiologicaldysfunctionofthemediannerve.Theassociationbetweencarpaltunnelsyndromeandulnarnerveentrapmentisstillunclear.Inthisstudy,wemeasuredulnarnervefunctionin82patientswithcarpaltunnelsyndrome.ThepatientsweredividedintogroupIwithminimalcarpaltunnelsyndrome(n=35)andgroupIIwithmildtomoderatecarpaltunnelsyndrome(n=47)accordingtoelectrophysiologicaldata.Sixty-oneage-andsex-matchedsubjectswithoutcarpaltunnelsyndromewereusedasacontrolgroup.Therewerenosignificantdifferencesinulnarsensorynervepeaklatenciesorconductionvelocitiesfromthe4thand5thfingersbetweenpatientswithcarpaltunnelsyndromeandthecontrolgroup.Theulnarsensorynerveactionpotentialamplitudesfromthe4thand5thfingerswerelowerinpatientswithcarpaltunnelsyndromethaninthecontrolgroup.Theratiosoftheulnarsensorynerveactionpotentialamplitudesfromthe4thand5thfingerswerealmostthesameinpatientswithcarpaltunnelsyndromeasinthecontrolgroup.Thesefindingsindicatethatinpatientswithminimaltomoderatecarpaltunnelsyndrome,thereissomeelectrophysiologicalevidenceoftractionontheadjacentulnarnervefibers.Thefindingsdonotindicateaxonaldegenerationoftheulnarnerve.
简介:无
简介:Familialdysautonomia(FD)isararechildrenneurodegenerativediseasecausedduetoapointmutationintheIKBKAPgenethatresultsindecreasedIKKcomplex-associatedprotein(IKAP)proteinproduction.Thediseaseaffectsmostlythedorsalrootganglion(DRG)andthesympatheticganglion.Recently,wefoundthatthemolecularmechanismsunderlyingneurodegenerationinFDpatientsaredefectsinaxonaltransportofnervegrowthfactorsandmicrotubulestabilityintheDRG.Neuronsarehighlypolarizedcellswithverylongaxons.Inordertosurviveandmaintainproperfunction,neuronsdependontransportofproteinsandothercellularcomponentsfromtheneuronalbodyalongtheaxons.WefurtherdemonstratedthatIKAPisnecessaryforaxonmaintenanceandshowedthatphosphatidylserineactsasanHDAC6inhibitortorescueneuronalfunctioninFDcells.Inthisreview,wewillhighlightourlatestresearchfindings.
简介:TheRho/Rho-associatedcoiled-coilcontainingproteinkinase(Rho/ROCK)pathwayisamajorsignalingpathwayinthecentralnervoussystem,transducinginhibitorysignalstoblockregeneration.Aftercentralnervoussystemdamage,themaincauseofimpairedregenerationisthepresenceoffactorsthatstronglyinhibitregenerationinthesurroundingmicroenvironment.ThesefactorssignalthroughtheRho/ROCKsignalingpathwaytoinhibitregeneration.Therefore,athoroughunderstandingoftheRho/ROCKsignalingpathwayiscrucialforadvancingstudiesonregenerationandrepairoftheinjuredcentralnervoussystem.
简介:Objective:Toobservetheeffectsofcryopreservedolfactoryensheathingcells(OECs)transplantationonaxonalregenerationandfunctionalrecoveryfollowingspinalcordinjuryinadultrats.Methods:Twenty-fourratsweredividedintoexperimentalandcontrolgroups,eachgrouphaving12rats.ThespinalcordinjurywasestablishedbytransectingthespinalcordatT10levelwithmicrosurgeryscissors.OECswerepurifiedfromSDratolfactorybulbandculturedinDMEM(Dulbecco'sminimumessentialmedium)andcryopreserved(-120℃)fortwoweeks.OECssuspension[(1-1.4)×105/ul]wastransplantedintotransectedspinalcord,whiletheDMEMsolutionwasinjectedinsteadinthecontrolgroup.At6and12weeksaftertransplantation,theratswereevaluatedwithclimbingtestandMEP(moterevokedpotentials)monitoring.Thesamplesofspinalcordwereprocuredandstudiedwithhistologicalandimmunohistochemicalstainings.Results:At6weeksaftertransplantation,alloftheratsinbothtransplantedandcontrolgroupswereparaplegic,andMEPscouldnotberecorded.MorphologyoftransplantedOECswasnormal,andOECswereinterfusedwithhostwell.Axonscouldregrowintogaptissuebetweenthespinalcords.BothOECsandregrownaxonswereimmunoreactiveforMBP.Noregrownaxonswerefoundinthecontrolgroup.At12weeksaftertransplantation,2rats(2/7)hadlowerextremitiesmusclecontraction,2rats(2/7)hadhipand/orkneeactivemovement,andMEPof5rats(5/7)couldberecordedinthecalfinthetransplantationgroup.Noneoftherats(7/7)inthecontrolgrouphadfunctionalimprovement,andnonehadMEPsrecorded.Inthetransplantedgroup,histologicalandimmunohistochemicalmethodsshowedthenumberoftransplantedOECsreducedandsomeregrownaxonshadreachedtheendoftransectedspinalcord.However,noregrownaxonscouldbeseenexceptscarformationinthecontrolgroup.Conclusions:CryopreservedOECscouldintegratedwiththehostandpromoteregrowingaxonsacrossthetransectedsp
简介:Objective:Toexplorethecontentchangeofneurofilament(NF)proteinsubunitsintheexperimentalbraindiffuseaxonalinjury(DAI)bylateralheadrotation.Methods:Twenty-fourSpragueDawley(SD)ratswereequallydividedintothreeinjurygroups(2h,12h,and24hpostinjury)andonecontrolgroup.ThemodelsofDAIweremadeintheinjurygroupsbylateralheadrotation.westernblottingtechniquewasusedtomeasuretheconteneofNF68(akindofNFproteinsubunit)inthebrainstemtissuesamongalltheinjuredandcontrolrats.TheNF68immunohistochemicalstainingwasusedinanothersixSDratsinordertoobservethemorphologicalchangesinDAI.Results:TheNF68contentinthebrainstemtendedtodecreaseat2hpostinjury,decreasedsignificantlyat12handcontinueditsdecreaseat24h.NF56andNF52,asthebreakdownproductsofNF68,hadatendencytoincreaseat2-12haftertheinjury,andamountedtoasignificantlyhigherlevelat24h.Microscopically,therewerealotofswellingneuronalaxonsintheventralpartofthemedullaroblongateat2haftertheinjury.someaxonsweredisconnected,andaxonalretractionballsformedontheirproximalend.Conclusions:ThereisandoccurrenceofphosphorolysiswithinthebrainsteminDAIbylateralheadrotation.ThesereactionscausethebreakdownofNF68,whichresultsinthedecreaseofNF68incontent.ItsuggeststhatthebreakdownofneurofilamentproteinsubunitsisanimportantreasonforstructuraldestroyofneurofilamentsinDAI.
简介:BACKGROUND:Previousstudieshaveshownthatp75neurotrophinreceptorplaysanimportantroleinperipheralnerveinjury.However,theroleofp75neurotrophinreceptorintheregenerationofperipheralnervesremainspoorlyunderstood.OBJECTIVE:Tostudytheeffectofp75neurotrophinreceptoronfacialnerveregeneration.DESIGN,TIMEANDSETTING:ArandomizedcontrolledexperimentwasperformedintheRegenerationLaboratoryofFlindersUniversity,AustraliaandtheBiomedicalLaboratoryofDentistrySchool,ShandongUniversityfromMarch2005toFebruary2006.MATERIALS:CholeratoxinBsubunit,fastblue,andbiotinrabbit-antigoatIgGwereprovidedbySigma,USA;goat-anticholeratoxinBsubunitantibodywasprovidedbyListBiologicals,USA.METHODS:Inp75neurotrophinreceptorknockoutandwildtype129/svmice,thefacialnervesononesidewerecrushed.Atdays2and4followinginjury,regeneratingmotorneuronsinthefacialnucleiwerelabeledbyfastblue,andtheregeneratingaxonwaslabeledbytheanterogradetracercholeratoxinBsubunit.MAINOUTCOMEMEASURES:AxonalregenerativevelocityandnumberweredetectedbyimmunohistochemicalstainingofcholeratoxinBsubunit,growth-associatedprotein,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptide;survivalofmotorneuronsinthefacialnucleiwasdetectedbyretrogradefastblue.RESULTS:Axonalgrowthinthefacialnerveofp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice.Atday7afterinjury,thenumberofregeneratingmotorneuronsinp75neurotrophinreceptorknockoutmiceremainedsignificantlylessthaninwildtypemice(P<0.05).Thenumberofpositivelystainedfibersforgrowth-associatedprotein-43,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptideinp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice(P<0.01).CONCLUSION:p75neurotrophinreceptorpromotedaxonalregenerationandenhancedthesurvivalrateofmotorneuronsfollowingfacialnerveinjury.
简介:ThepresentstudyestablishedachronicexperimentalautoimmuneencephalomyelitismodelinC57BL/6miceinducedbymyelinoligodendrocyteglycoproteinpeptidesandcompleteFreund'sadjuvant.Onsetlatencywas12days,withanincidencerateof100%.Neuropathologicalcharacteristicsincludedperivascularinflammatorycellinfiltration,demyelination,neuronaldegeneration,andaxonaldamagewithincerebralandmyelicwhitematter.Electronmicroscopyrevealedswollenmitochondria,completeorgandisappearance,andfusedorbrokenmyelinsheathstructure,whichwereaccompaniedbymyelinsheathreconstruction.Moreover,axonaldamagewasnotconsistentwithdemyelinationdistribution,andseverityofaxonaldamagedidnotcorrelatewithdemyelination.Resultssuggestedthataxonaldamageinanexperimentalautoimmuneencephalomyelitismodelisnotsecondarytoinflammatorydemyelination.