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

简介：BACKGROUND:Previousstudieshaveshownthatthemitochondrialstructureandfunctionaredamagedinanimalmodelsofepilepsy.Inaddition,theBcl-2proteiniscapableofregulatingmitochondrialstability.OBJECTIVE:ToobserveandvalidatechangesinmitochondrialstructureandBcl-2expression,andtoanalyzethesecharacteristicsinthehippocampalCA3regionofratmodelsofepilepsy.DESIGN,TIMEANDSETTING:Thisrandomized,controlled,animalexperimentwasperformedattheLaboratoryofElectronMicroscopyandDepartmentofHistologyandEmbryology,LuzhouMedicalCollegebetween2007and2008.MATERIALS:CoriamyrtinwasprovidedbythePharmacyFactoryofWestChinaUniversityofMedicalSciences.TheprimaryandsecondaryantibodieswereprovidedbyZhongshanGoldenbridgeBiotechnology,Beijing.METHODS:Atotalof44adult,male,SpragueDawleyratswererandomlydividedintocontrol(n=11)andepilepsy(n=33)groups.Ratsintheepilepsygroupwereinducedbycoriamyrtin(50μg/kg),whichwasinjectedintothelateralventricles.Theratswerethenobservedat3,6,and24hoursafterepilepsyinduction,with11ratsateachtimepoint.Epilepsywasnotinducedinratsfromthecontrolgroup.MAINOUTCOMEMEASURES:PathologicalchangesinthehippocampalCA3regionwereobservedbylightmicroscopy;Bcl-2expressionwasanalyzedbyimmunohistochemistry;andmitochondrialchangesinthehippocampuswereobservedundertransmissionelectronmicroscopy.RESULTS:(1)ThecontrolgroupdisplayedverylittleBcl-2proteinexpressioninthehippocampalCA3region.However,after3hoursofepilepsy,expressionwasvisible.By6hours,expressionpeakedandthensubsequentlydecreasedafter24hours,butremainedhigherthanthecontrolgroup(P<0.05).(2)Mitochondriaweredamagedtovaryingdegreesintheepilepsygroups.Forexample,mitochondriaedema,cristaespaceincrease,anddisappearanceofmitochondriawereapparent.Moreover,mitochondrialdamageoccurredpriortopathologicalchangesintheneuronsandnucleolus.CONCLUSION:

简介：BACKGROUND:Animalexperimentshaveconfirmedthatbonemarrowstromalcell(BMSC)transplantationcanserveasatreatmentforepilepsy.OBJECTIVE:BMSCsderivedfromgreenfluorescentprotein(GFP)miceweretransplantedintothehippocampalCA1regionofepilepticrats.Theaimofthestudywastorecordelectroencephalogram(EEG),analyzesurvivalandmigrationofBMSCs,andvalidatetheeffectofBMSCtransplantationforthetreatmentofepilepsy.DESIGN,TIMEANDSETTING:ArandomizedblockdesignexperimentwasperformedattheInstituteofNeuroscience,KunmingMedicalCollegefromMarch2005toFebruary2006.MATERIALS:HomozygousC57BL/6CrSlcTgN(acr-EGFP)OsbC14-Y01-FM131mice,8-12weeksofage,wereselectedforpreparationofcellsuspension.SpragueDawleyratswereselectedforestablishingepilepsymodels.METHODS:Ratswererandomlydividedinto4groups:control(n=8),model(n=8),normalsaline(n=24),andBMSC(n=24).Inthemodel,normalsaline,andBMSCgroups,epilepsywasestablishedwithpenicillin(3×107U/kgi.p.×7days).RatsintheBMSCgroupreceivedaBMSCsuspensionderivedfromgreenfluorescentproteinmiceintotherighthippocampalCA1region.RatsinthevehiclecontrolgroupwereinjectedwiththesamevolumeofnormalsalineintothehippocampalCA1region.MAINOUTCOMEMEASURES:Theelectroencephalogramwasusedtomonitorbrainactivity.SurvivalandmigrationofthetransplantedBMSCswasobservedusingfluorescencemicroscopyat1,2,and4weeksaftertransplantation.RESULTS:InBMSCgroup,fluorescentcellswereobservedatthetransplantationsiteandintheadjacenttissue,aswellasinthetissuesurroundingtheneedletract,indicatingthemigrationofimplantedcells.Fluorescentcellswerenotdetectedinthevehiclecontrolgroup.Theelectroencephalogramofthecontrolanimalsexhibited7-9Hzαwaves,withawaveamplitude<50μV.Inthemodelandvehiclecontrolgroups,randomspike-and-wavedischargesofthesharpspike-sharplowwavetyp

简介：BACKGROUND:Calciumion(Ca2+)overloadplaysanimportantroleincerebralischemia/reperfusioninjury.Anisodamine,atypeofalkaloid,canprotectthemyocardiumfromischemiaandreperfusioninjurybyinhibitingintracellularcalcium[Ca2+]ioverload.OBJECTIVE:Toinvestigateeffectsofanisodamineon[Ca2+]iconcentrationandcortexultrastructurefol-lowingacutecerebralischemia/reperfusioninrabbits.DESIGN,TIMEANDSETTING:RandomizedandcontrolledtrialwasperformedattheDepartmentofEmergency,TongjiHospital,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnologyfromSeptembertoDecember2006.MATERIALS:Fortyhealthyrabbitswereusedtoestablishmodelsofacutecerebralischemia/reperfusion.AnisodaminewasprovidedbyLianyungangDongfengPharmaceuticalFactory;Fura-2waspurchasedfromNanjingJianchengBioengineeringInstitute;dual-wavelengthfluorescentspectrophotometrysystemandDM-300softwarewereprovidedbyBio-Rad,USA;OPTON-EM10CtransmissionelectronmicroscopewasproductofSiemens,Germany.METHODS:Fortyrabbitswererandomlydividedintothefollowinggroups:shamoperation,ischemia,ischemia/reperfusion,andanisodamine,withtenrabbitsineachgroup.Modelsofcompletecerebralischemiainjurywereestablished.Inaddition,bloodwascollectedfromthefemoralarteryofratsintheischemia/reperfusionandanisodaminegroupstoinducehypotensionandestablishreperfusioninjurymodels.Thebilateralcommoncarotidarteryclampwasremovedfromtheanisodaminegroup20minutesafterischemia,andanisodamine(10mg/kgbodymass)wasinjectedviathefemoralvein.Rabbitsintheshamoperationgroupunderwentonlyvenouscannulation.MAINOUTCOMEMEASURES:[Ca2+]iconcentrationwasdeterminedusingadual-wavelengthfluorescentspectrophotometrysystem,andcorticalultrastructurewasobservedfollowinguranyl-leadcitratestaining.RESULTS:Thelevelsof[Ca2+]iintheischemiaandischemia/reperfusiongroupsweresignificantlyin-creased,c

简介：Heatshockprotein70(HSP70)maintainsCa~(2+)homeostasisinPC12cells,whichmayprotectagainstapoptosis;however,themechanismsofneuroprotectionareunclear.Therefore,inthisstudy,weexaminedCa~(2+)levelsinPC12cellstransfectedwithanexogenouslentiviralHSP70geneexpressionconstruct,andwesubsequentlysubjectedthecellstoischemia-hypoxia/reoxygenationinjury.HSP70overexpressionincreasedneuronalviabilityandATPaseactivity,anditdecreasedcellularreactiveoxygenspecieslevelsandintracellularCa~(2+)concentrationafterhypoxia/reoxygenation.HSP70overexpressionenhancedtheproteinandmRNAexpressionlevelsofsarcoplasmic/endoplasmicreticulumCa~(2+)-ATPase(SERCA),butitdecreasedtheproteinandmRNAlevelsofinositol1,4,5-trisphosphatereceptor(IP3R),therebyleadingtodecreasedintracellularCa~(2+)concentrationafterischemia-hypoxia/reoxygenation.TheseresultssuggestthatexogenousHSP70protectsagainstischemia-hypoxia/reoxygenationinjury,atleastinpart,bymaintainingcellularCa~(2+)homeostasis,byupregulatingSERCAexpressionandbydownregulatingIP_3Rexpression.

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.

简介：目的观察胰岛素对全脑缺血后海马CA1区神经元凋亡及大鼠学习记忆力改变的影响,探讨胰岛素对全脑缺血后海马CA1区神经元产生中枢直接保护作用的机理.方法利用4-VO法制作大鼠全脑缺血模型.造成脑缺血15min后行再灌注,于再灌注后即刻经脑室注入1U胰岛素,利用免疫组化及原位标记法分别于全脑缺血后1、3d观察海马CA1区Bcl-2、Bcl-xl蛋白表达及神经元凋亡的情况;缺血后8周,利用"Y"型迷宫测试大鼠的学习记忆功能.结果全脑缺血后3d,缺血组大鼠海马CA1区Bcl-2、Bcl-xl蛋白的表达呈阴性,海马CA1区原位标记阳性细胞计数为143.5±11.6.治疗组大鼠海马CA1区Bcl-2、Bcl-xl蛋白呈阳性表达,海马CA1区原位标记阳性细胞计数为75.6±6.7.全脑缺血后8周,治疗组大鼠学习记忆力明显好于缺血组.结论全脑缺血后脑室内注入胰岛素可促进海马CA1区Bcl-2、Bcl-xl蛋白表达,减少神经元的凋亡,进而减轻脑缺血后大鼠的学习记忆力损害,这可能是其对全脑缺血后海马CA1区神经元产生中枢直接保护作用主要机理之一.

简介：Ischemicpreconditioningelicitedbyanon-fatalbriefocclusionofbloodflowhasbeenappliedforanexperimentaltherapeuticstrategyagainstasubsequentfatalischemicinsult.Inthisstudy,weinvestigatedtheneuroprotectiveeffectsofischemicpreconditioning(2-minutetransientcerebralischemia)oncalbindinD28kimmunoreactivityinthegerbilhippocampalCA1areafollowingasubsequentfataltransientischemicinsult(5-minutetransientcerebralischemia).AlargenumberofpyramidalneuronsinthehippocampalCA1areadied4daysafter5-minutetransientcerebralischemia.IschemicpreconditioningreducedthedeathofpyramidalneuronsinthehippocampalCA1area.CalbindinD28kimmunoreactivitywasgreatlyattenuatedat2daysafter5-minutetransientcerebralischemiaanditwashardlydetectedat5dayspost-ischemia.IschemicpreconditioningmaintainedcalbindinD28kimmunoreactivityaftertransientcerebralischemia.Thesefindingssuggestthatischemicpreconditioningcanattenuatetransientcerebralischemia-causeddamagetothepyramidalneuronsinthehippocampalCA1areathroughmaintainingcalbindinD28kimmunoreactivity.

简介：Thepresentstudywasdesignedtodeterminemicrotubule-associatedprotein-2andsynaptophysinexpressioninthehippocampalCA3regioninaratmodelofmiddlecerebralarteryocclusion.TheratsweretreatedwithacupunctureatBaihui(GV20),Qubin(GB7),andQianding(GV21)points,inadditiontoexercisetraining.Resultswerecomparedwithratsundergoingexercisetrainingonly.TheY-mazemethodandimmunohistochemistryrevealeddecreasederrorfrequencyofpassingthroughY-maze,aswellassignificantlyincreasedmicrotubule-associatedprotein-2andsynaptophysinexpression,intheacupuncturewithexercisetraininggroupcomparedwiththemodelandexercisetraininggroupsafter5weeks.Microtubule-associatedprotein-2andsynaptophysinexpressionsnegativelycorrelatedwitherrorfrequencyofpassingthroughtheY-maze.Theseresultssuggestedthatacupuncturecombinedwithexercisetrainingimprovedlearningandmemoryfunctionsinaratmodelofcerebralinfarction.ThemechanismsofactionwerehypothesizedtobeassociatedwithdendriticorsynapticplasticityintheipsilateralhippocampalCA3region.