中南大學(xué)湘雅醫(yī)學(xué)院，生理課件，細(xì)胞生理功能(編輯修改稿)
2025-01-31 03:51 本頁面
【文章內(nèi)容簡介】 Na. VoltageDependence of Conductance How channel conductances accumulate Next page shows an idealized version All or None character of action potential The amplitude of AP do not vary with stimulating intensity digital signal The amplitude of AP do not decline during propagating Variation of excitability on different membrane potential level ： absolute refractory period: no any response relative refractory period: weak response subnormal period: hyporesponse supranormal period: hyperresponse Depend on states of Na channels and distance between Em and threshold potential Slide 3 of 28 m m m h m m m h m m m h inactivation activation 1ms recovery Repolarization to RP depolarization automatically Resting state Active state Inactive state Genesis and propagation of action potential threshold membrane potential the membrane potential which is the lowest level of depolarization to induce a AP and at which the rate of Na channel activating is just counteract the rate of K outward current. local potential or local response Conception: subthreshold stimuli—induced a small and shortlived depolarization of membrane potential. * Dependent of stimulatingintensity * Declineelectrotonic propagation * Without refractory period * Summation: temporal and spatial Propagation of the Action Potential Factors that affect the propagation ? Bioelectric properties of the membrane ? Velocity and amplitude of membrane depolarization Saltatory Conduction Saltatory Conduction ? The pattern of conduction in the myelinated nerve fiber from node to node ? It is of value for two reasons: ? very fast ? conserves energy. Part Ⅲ Contraction of Muscle Cells Skeletal Muscle Cardiac Muscle Smooth Muscle Classification of the Muscle Signal Transmission Through the Neuromuscular Junction Skeletal Muscle Innervation Illustration of the Neuromuscular Junction (NMJ) K+ Outside Inside Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ K+ K+ K+ K+ K+ K+ K+ K+ K+ K+ K+ ACh ACh ACh Ca2+ induces fusion of vesicles with nerve terminal membrane. ACh is released and diffuses across synaptic cleft. ACh ACh binds to its receptor on the postsynaptic membrane Binding of ACh opens channel pore that is permeable to Na+ and K+.Na+ Na+ K+ Muscle membrane Ca2+ Ca2+ End Plate Potential (EPP) Outside Inside Muscle membrane Presynaptic terminal Muscle Membrane Voltage (mV) Time (msec) 90 mV VK VNa 0 Threshold Presynaptic AP EPP The movement of Na+ and K+ depolarizes muscle membrane potential (EPP) ACh Receptor Channels Voltagegated Na Channels Inward Rectifier K Channels Meanwhile ... Outside Inside ACh ACh unbinds from its receptor Muscle membrane ACh so the channel closes ACh ACh ACh is hydrolyzed by AChE into Choline and acetate Choline Acetate Choline is taken up into nerve terminal Choline Choline resynthesized into h and repackaged into vesicle ACh Neuromuscular Transmission ? Properties of neuromuscular junction ? 1:1 transmission: A chemical transmission which is designed to assure that every presynaptic action potential results in a postsynaptic one ? An unidirectional process ? Has a time delay. 20nm/ ? Is easily affect by drugs and some factors ? The NMJ is a site of considerable clinical importance Anticholinesterase Agents ? Anticholinesterase (antiChE) agents inhibit acetylcholines
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鄂ICP備17016276號-1