神学5

Question1:Whatismeantbyquantalreleaseofneurotransmitter?Answer:Theelementaryunitofaneurotransmitterreleaseisthecontentofonesynapticvesicle.Eachvesiclecontainsseveralthousandtransmittermolecules.Thetotalamountoftransmitterreleasedatasynapseisamultipleofthisnumber,dependingonhowmanyvesiclesreleasetheircontentsintothesynapticcleft.TheamplitudeofpostsynapticEPSPisamultipleoftheresponsetothecontentsofonevesicle.Itreflectsthenumberoftransmittermoleculesinonesynapticvesicleandthenumberofpostsynapticreceptorsavailableatthesynapse.一个神经递质释放的基本单位是一个突触囊泡的内容物。每个囊泡包含几千个神经递质分子。在突触释放神经递质的总数是这个数目的倍数，并取决于多少囊泡释放到突触间隙的内容。因此突触后EPSP的反应幅度是一个囊泡的内容物的整数倍。它反映了一个突触小泡的递质分子的数量和突触中可用的突触受体的数量。Question2:YouapplyAChandactivatenicotinicreceptorsonamusclecell.WhichwaywillcurrentflowthroughthereceptorchannelswhenVm=–60mV?WhenVm=0mV?WhenVm=60mV?Why?Answer:NicotonicAChreceptorsarepermeabletobothsodiumandpotassium.WhenVm=–60mV,netcurrentflowthroughACh-gatedionchannelsisinward,towardtheequilibriumpotentialofsodium,causingdepolarization.AtVm=60mV,thedirectionofnetcurrentflowthroughtheACh-gatedionchannelsisoutward,towardtheequilibriumpotentialofpotassium,causingthemembranepotentialtobecomelesspositive.Thecriticalvalueofmembranepotentialatwhichthedirectionofcurrentflowreversesiscalledthereversalpotential.Inthiscase,thereversalpotentialis0mVbecausethisisthevaluebetweentheequilibriumpotentialsofsodiumandpotassium.At0mV,nocurrentflows.尼古丁型乙酰胆碱受体渗透钠和钾。当Vm=–60mV时，通过乙酰胆碱门控离子通道的电流流方向向内，向钠平衡电位移动，造成去极化。在Vm=60mV，通过乙酰胆碱门控离子通道的净电流方向向外，向钾平衡电位移动，导致膜电位超极化。在膜电流方向的逆转处，膜电位的值被称为逆转电位。在题设情况下，逆转电位为0mV的，因为膜对钠离子和钾离子的通透性相同。在Vm=0mV时，没有电流流过。Question3:Inthischapter,wediscussedaGABA-gatedionchannelthatispermeabletoCl–.GABAalsoactivatesaG-protein-coupledreceptorcalledtheGABAβreceptor,whichcausespotassium-selectivechannelstoopen.WhateffectwouldGABAβreceptoractivationhaveonthemembranepotential?Answer:ActivatedGABA-gatedCl–ionchannelsbringthemembranetowardtheequilibriumpotentialforCl–,whichis–65mV.Ifthemembranepotentialwaslessnegativethan–65mVwhenthetransmitterwasreleased,activationwouldcausehyperpolarization.TheactivationofGABAβreceptorscausespotassium-selectivechannelstoopen.Asaresult,GABAβactivationbringsmembranepotentialtowardtheequilibriumpotentialofpotassium,whichis–80mV.Ifthemembranepotentialwaslessnegativethan–80mVwhenthetransmitterwasreleased,activationwouldalsocausehyperpolarization.Thischannelmightalsoimpacttheneuronbyshuntinginhibition,allowingadepolarizingcurrentfromanexcitatorysynapsetoleakout.This,inturn,decreasesthelikelihoodofactionpotential.TheactionofaG-protein-coupledreceptoris,however,slowerthanthatoftheGABA-gatedCl–ionchanneloratypicalexcitatorysynapse.Therefore,itseffectswouldbeslowertooccurandwouldlastlonger.激活GABA门控氯离子通道，使膜电位向Cl-平衡电位移动，即-65毫伏。如果当递质释放时，膜电位小于-65mV，激活通道会导致超极化。GABAβ受体激活导致选择性钾通道开放。因此，GABAβ激活使膜电位向钾的平衡电位移动，即-80mV。如果当递质释放时，膜电位大于-80mV，激活也会导致超极化。这可能也会影响渠道分流抑制神经元，允许兴奋性突触的去极化电流泄露。这反过来，降低动作电位的可能性。G蛋白偶联受体的作用，比GABA门控氯离子通道或一个典型的兴奋性突触慢。因此，它产生效果会比较慢，但将持续更长的时间。Question4:Youthinkyouhavediscoveredanewneurotransmitter,andyouarestudyingitseffectonaneuron.Thereversalpotentialfortheresponsecausedbythenewchemicalis–60mV.Isthissubstanceexcitatoryorinhibitory?Why?Answer:Ifthenewchemicalhasareversalpotentialof–60mV,thesubstanceislikelytobeinhibitory.Thereversalpotentialreflectsthetypesofionsthemembraneispermeabletoaftertheapplicationoftheneurotransmitter.Areversalpotentialof–60mVsuggeststhattheneurotransmitteractivatesionchannelsthatmakethemembranemorenegative.Ifaneurotransmittercausesthemembranetomovetowardavaluethatismorenegativethantheactionpotentialthreshold,theneuronbecomeslesslikelytofireanactionpotential,whichmeansitisinhibited.如果新的化学物质的逆转电位为-60mV，该化学物质可能为抑制性。逆转电位反映神经递质释放后膜通透的离子种类。-60mV的逆转电位表明，神经递质激活的离子通道使膜电位更负。如果一种神经递质，导致膜电位朝比动作电位的阈值更负的值移动时，神经元触发一个动作电位的可能降低，这意味着该递质为抑制性。Question5:Adrugcalledstrychnine,isolatedfromtheseedsofatreenativeinIndiaandcommonlyusedasratpoison,blockstheeffectsofglycine.Isstrychnineanagonistoranantagonistoftheglycinereceptor?Answer:Strychnineisanantagonistofglycineatitsreceptor.Mildstrychninepoisoningenhancesthestartleandotherreflexesandresembleshyperekplexia.Highdosescaneliminateglycine-mediatedinhibitionincircuitsofthespinalcordandthebrainstem.Thisleadstouncontrollableseizuresanduncheckedmuscularcontractions,spasms,andparalysisofrespiratorymuscles.Itmightultimatelyresultinpainful,agonizingdeathfromasphyxiation.Strychnine是一个甘氨酸受体的拮抗剂。轻度的Strychnine中毒增强了惊吓和其他反射并和夸大的警报反映相似。高剂量的Strychnine可以消除甘氨酸介导的对脊髓和脑干回路的抑制作用。这将导致无法控制的癫痫和肌肉收缩，痉挛，呼吸肌麻痹。它最终可能会导致窒息死亡。Question6:Howdoesnervegascauserespiratoryparalysis?Answer:NervegasesinterferewithsynaptictransmissionattheneuromuscularjunctionbyinhibitingAChE.UninterruptedexposuretohighconcentrationsofAChforseveralsecondsleadstoaprocesscalleddesensitization.Inthisprocess,transmitter-gatedchannelsclosedespitethecontinuedpresenceofACh.Normally,therapiddestructionofAChbyAChEpreventsdesensitization.However,ifAChEisinhibitedbynervegas,AChreceptorswillbedesensitizedandneuromusculartransmissionwillfail,causingrespirato