简介：Inthisstudy,ratswereputintotraumaticbraininjury-inducedcomaandtreatedwithmediannerveelectricalstimulation.Weexploredthewake-promotingeffect,andpossiblemechanisms,ofmediannerveelectricalstimulation.Electricalstimulationupregulatedtheexpressionlevelsoforexin-AanditsreceptorOX1Rintheratprefrontalcortex.Orexin-Aexpressiongraduallyincreasedwithincreasingstimulation,whileOX1Rexpressionreachedapeakat12hoursandthendecreased.Inaddition,aftertheOX1Rantagonist,SB334867,wasinjectedintothebrainofratsaftertraumaticbraininjury,fewerratswererestoredtoconsciousness,andorexin-AandOXIRexpressionintheprefrontalcortexwasdownregulated.Ourfindingsindicatethatmediannerveelectricalstimulationinducedanup-regulationoforexin-AandOX1Rexpressionintheprefrontalcortexoftraumaticbraininjury-inducedcomarats,whichmaybeapotentialmechanisminvolvedinthewake-promotingeffectsofmediannerveelectricalstimulation.

简介：Vagusnervestimulationexertsprotectiveeffectsagainstischemicbraininjury;however,theunderlyingmechanismsremainunclear.Inthisstudy,aratmodeloffocalcerebralischemiawasestablishedusingtheocclusionmethod,andtherightvagusnervewasgivenelectricalstimulation(constantcurrentof0.5mA;pulsewidth,0.5ms;frequency,20Hz;duration,30seconds;every5minutesforatotalof60minutes)30minutes,12hours,and1,2,3,7and14daysaftersurgery.Electricalstimulationofthevagusnervesubstantiallyreducedinfarctvolume,improvedneurologicalfunction,anddecreasedtheexpressionlevelsoftumornecrosisfactor-αandinterleukin-6inratswithfocalcerebralischemia.Theexperimentalfindingsindicatethattheneuroprotectiveeffectofvagusnervestimulationfollowingcerebralischemiamaybeassociatedwiththeinhibitionoftumornecrosisfactor-αandinterleukin-6expression.

简介：Brief-pulsestimulationat50Hzhasbeenshowntoterminateafterdischargesobservedinepilepsypatients.However,theoptimalpulsestimulationparametersforterminatingcorticalelectricalstimulation-inducedafterdischargesremainunclear.Inthepresentstudy,weexaminedtheeffectsofdifferentbrief-pulsestimulationfrequencies(5,50and100Hz)oncorticalelectricalstimulation-inducedafterdischargesin10patientswithrefractoryepilepsy.Resultsdemonstratedthatbrief-pulsestimulationcouldterminatecorticalelectricalstimulation-inducedafterdischargesinrefractoryepilepsypatients.Inconclusion,(1)abrief-pulsestimulationwasmoreeffectivewhentheafterdischargedidnotextendtothesurroundingbrainarea.(2)Ahigherbrief-pulsestimulationfrequency(especially100Hz)wasmorelikelytoterminateanafterdischarge.(3)Alowcurrentintensityofbrief-pulsestimulationwasmorelikelytoterminateanafterdischarge.

简介：Aratmodelofextra-vertebralforamencervicalnerveentrapmentwasestablishedaccordingtothefollowingparameters:stimulationintensity20V;frequency50Hz;pulsewidth200μs;duration333ms/sforatotalof8hours.Aftertheelectricalstimulation,ratsexhibitedmildmusclefiberatrophy,mildinflammatoryexudates,connectivetissuelocalfibrosisandchondrocytemetaplasia.Meanmusclefibercross-sectionalareawasreduced.Thenervemyelinsheathcontinuitywaspartiallydemyelinated.Themicrostructureofnervecellswasdisruptedandthesesymptomsworsenedwithprolongationofthestimulation.Theshoulder,neckandupperextremitymusclesonthetestedsidedemonstratedpositivesharpwavesandfibrillations.Theseverityincreasedwithcontinuationofthestimulation.Highamplitudeandpolyphasicmotorunitpotentialsgraduallyappeared.Similarfindingswereseeninthecontralateralside,butatalessseverelevel.