第二十章一骨骼肌神经-接头传递

六、肌细ContractionofMuscle(肌束(肌纤维/肌细胞(肌原纤维(肌节/肌小节(肌丝

Productionofbody运动单位(motor（一）骨骼肌神经-肌接头的传神经-肌接头（NMJ）微细接头前接头后膜或终板接头间神经肌接头（NMJ）兴奋传*ActivationofACh-gatedionchannel(nAChR)resultsinEnd-PlatePotential(EPP)神经肌接头传递（电-化学-电过程神经冲神经冲动到达末梢，接头前膜去电压门控Ca2＋通道开放、Ca2＋内囊泡向接头前膜囊泡向接头前膜移动、融合、破ACh释放至接头乙NaNa＋内流使终板膜去极化NMJ兴奋传递的特征是电-化学-电的N末梢AP→ACh＋受体→EPP→肌膜具1对1的关奋和收缩一次（因每次ACh释放的量，产生的影响NMJ兴奋传递的因素： 阻断ACh受体：箭毒(curare)α（Flexadil，三碘季胺酚） 新斯的明，Sarin,VX,etc。3自身免疫性疾病：Myasthenia（抗体破坏ACh受体),Lambert-Eatonsyndrome（抗体破坏N末梢Ca2+4接头前膜ACh释放↓：肉毒杆菌毒（二）横纹肌细胞的兴奋-收缩耦兴奋-收缩耦联的结构基道）Longitudinaltubularsystem：LTriad：T管+兴奋-收缩耦联的关键离子——L型钙通道和钙释放通骨骼肌细胞和心肌细胞的钙释骨骼肌细胞和心肌细胞的钙回钙瞬变（calciumtransient）引起肌肉的收缩和舒兴奋-①肌膜电兴奋的传导②肌膜和T管上L型Ca2+通道激活③肌浆网上Ryanodine受体激活，肌浆网Ca2+释放(calcium④触发肌丝滑行，肌细胞收缩（三）肌丝的分子组粗肌丝（thick肌球蛋白横桥（cross-

细肌丝（thin肌动蛋白原肌球蛋白肌钙蛋白（troponin横纹肌收缩的原理—Z

MlineHband

ZA直

白的相互ICT ICTs原肌球蛋白细肌丝上的结合肌肌节缩短,肌细胞收Sourcesof肌肉的舒张(Muscle—mechanismsthatrestoresarcoplamicBacktocalciumCa2+pumpinsarcoplasmicreticulum~100%inskeletal~70%incardiacOutofthe①Na+-Ca2+exchangerincell②Ca2+pumpincellDiseasesassociatedwithabnormalregulationtheintracellularCa2+inskeletal Malignanthyperthermia:geneticdefectinryanodinereceptor,1in15,000children,1in50,000adults;Halothane/etherorsuccinylcholinestimulateCa2+releasefromSR,resultingmusclerigidityandhyperthermiaCentralcoredisease:geneticdefectinryanodinereceptor;SRreleases/leakCa2+,whichisthenaccumulatedbymitochondria,resultinginmitochondrialCa2+overloadandhencelossofmitochondriaandmuscleweaknessBrody’sdisease:geneticdefectinSRCa2+pump(SERCA):painlessmusclecram duringexerciseduetoslowedCa2+Summary:SequentialeventsofThesarcolemmaisdepolarizedandtheactionpotential(AP)propagates;TheactionpotentialspreadsinsidealongtheT-tubules;APistransmittedfromT-tubuletoterminalsacsofsarcoplasmicreticulum;Calciumisreleasedfromsarcoplasmicreticulumintosarcoplasm;Calciumbindstotroponinleadingtocooperativeconformationalchangesintroponin-tropomyosinsystem;Theinhibitionofactinandmyosininteractionisreleased;Crossbridgesofmyosinfilamentsareattachedtoactinfilaments;Tensionisexertedand/orthemuscleshortensbytheslidingfilamentCalciumispumpedbackintosarcoplasmicreticulum;Crossbridgesaredetachedfromthethinfilaments;Troponin-tropomyosinregulatedinhibitionofactinandmyosininteractionisActivetensiondisappearsandtherestlengthis（四）影响横纹肌收缩效能的肌肉收缩的形单收缩、复合收缩、强直等张收IsotonicForce等长ForceIsometric单收缩、复合收缩与强直收 前负荷 后负荷(After-determineslengthofcross-bridge cyclesandhencetotalnumberofcross-bridgesinteractingwiththinfilaments;肌肉的收缩性 affectingthoseproperties前负荷（Preload)：肌肉收缩前所承受的负荷,决定了肌节最适初长（2.0-2.2m）时，粗细肌丝 佳，肌 小于最适初长时，细肌丝可缩短距离↓→效能↓大部分骨骼肌的静态长度即是其最适初长，Optimalinitiallength也称Resting肌 Optimalinitiallength(resting后负荷↓→肌缩速度、幅度↑和张力↓后负荷过大，虽肌缩张力↑，但肌缩速度↓，不利作功后负荷过小，虽肌缩速度、幅度↑，但肌↓，也不利作TypesofskeletalTypeImuscleTypeIImuscleOtherATPaserateofsarcoplasmicGlycolyticOxidativeFine,skilled（五）平滑肌的收缩和舒MorphologicalMorphologicalandfunctionalMechanismsof形态学特involuntarymuscle;innervatedbyANS;foundprimarilyinthewallsofhollowSpindle-shapedcellstypicallyarrangedinNot-tubules&littlesarcoplasmic eres(soarenotstriated)butaremadeupofthick&myofilaments.ThinfilamentsinsmoothmuscledonotcontainCalciumbindstocalmodulin.Thecalcium-calmodulincomplex'activates'myosinwhichthenbindstoactin&contraction(swivellingofcross-bridges)Twotypesofsmooth多个单位平滑visceral,orunitary,smoothfoundinthewallsofholloworgans(e.g.,smallbloodvessels,digestivetract,urinarysystem,&reproductivesystem)multiplefiberscontractasaunit(becauseimpulsestraveleasilyacrossgapjunctionsfromcelltocell)&,insomecases,areself-excitable(generatespontaneousactionpotentials&contractions)multiunitsmoothconsistsofmotorunitsthatareactivatedbynervousfoundinthewallsoflargebloodvessels,intheeye(adustingtheshapeofthelenstopermit modation&thesizeofthepupiltoadjusttheamountoflightenteringtheeye),&atthebaseofhairfollicle(the'goosebump'muscles)Openingofvoltage-gatedcalciumchannelsaccountsfortheactionpotentialofmostsmoothmusclecells.平滑肌收缩与舒IonLittleappreciatedfactofHumanbeings(andotherlivingorganisms)arerunbyelectricity,and"ionchannels"arethecoreofourelectricalIonchannelsareeverywhere&arepresentinalmosteveryTransportofionsandRegulationofelectricalpotentialacrosstheIonYetanothertypeofmembranePoresinthemembranethatopenandcloseinaregulatedmannerandallowpassageofions“Dispose”ofthe Passivetransporters:IonsflowfromhightolowNoenergyisused;IfthereisnogradientionswillnotflowChannelIonchannelsarenotopencontinuouslybutopenandcloseinastochasticorrandomfashion.Ionchannelfunctionmaybedecreasedbydecreasingtheopentime(o),increasingtheclosedtime(c),decreasingthesinglechannelcurrentamplitude(i)ordecreasingthenumberofchannels(n).Whatgatesionchannel