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Temporal excitatory summation: a series of impulses in one excitatoryfiber together produce a suprathreshold depolarization that triggers anaction potentialExcitatory fibersmVExcitatory fibersmVD. Spatial excitatory summation: impulses in two excitatory fibers causetwo synaptic depolarizations that together reach the firing threshold,triggering an action potentialExcitatory fibersmV–70–70AxonAxonInhibitory fibersInhibitory fibersE.
Spatial excitatory summation with inhibition: impulses from twoexcitatory fibers reach a motor neuron, but impulses from inhibitoryfiber prevent depolarization from reaching the thresholdE. (continued): the motor neuron now receives additional excitatoryimpulses and reaches firing threshold despite a simultaneous inhibitoryimpulse; additional inhibitory impulses might still prevent firingFigure 3.8 Temporal and Spatial Summation In the resting state (A), the nerve cell is at its restingmembrane potential.
Neurons are subject to multiple inhibitory and stimulatory signals that produce localpotential changes, which are subject to both temporal and spatial summation. The sum of these influencesdetermines whether an action potential is produced (B–E).receptor. The action of acetylcholine is rapid; it is also short-livedbecause acetylcholine diffuses out of the synaptic cleft or israpidly broken down by acetylcholinesterase localized on thebasement membrane of the muscle fiber.Binding of postsynaptic nicotinic receptors by acetylcholinecauses the opening of ligand-gated channels.
Influx of Na+and K+ through these channels produces an excitatory postsynaptic potential (endplate potential). When this endplatepotential reaches threshold, an action potential is generated,ultimately producing contraction of the muscle fiber. Pharmacologically, the actions of acetylcholine can be blocked bycurare, a competitive antagonist that binds reversibly to thenicotinic receptor, thereby blocking acetylcholine binding, orby cobra venom (α-bungarotoxin), a noncompetitive antagonist that binds irreversibly to the receptor.Endplate potentials differ from neuronal action potentials inseveral important ways:■■Endplate potentials are produced by a ligand-gatedchannel; neuronal action potentials are caused byvoltage-gated channels.
In both cases, the action potential is generated in the postsynaptic cell when a thresholdis reached.Rapid depolarization, to a potential of 0 mV, comparedwith rapid depolarization to +40 mV during a neuronalaction potential.Nerve and Muscle PhysiologyI(Inhibitoryfiber)E(Excitatory fiber)MotorneuronmV20A.
Only E fires90-mV spike in E terminalE(Excitatory fiber)MotorneuronI(Inhibitory fiber)AxonAxonmV90 mVA′. Only E firesEPSP in motor neuron607060EPSP in motor neuronB. Only I firesLong-lasting partial depolarizationin E terminalNo response in motor neuron7070B′. Only I firesMotor neuron hyperpolarized6070708070C. I fires before E20Partial depolarization of E terminalreduces spike to 80 mV, thusreleasing less transmitter substance80 mV7060Smaller EPSP in motor neuron37C′. I fires before EDepolarization of motorneuron less than if only E fires60708070Figure 3.9 Synaptic Inhibitory Mechanisms Inhibition can occur through either presynaptic orpostsynaptic mechanisms. In presynaptic inhibition, illustrated (top left) for a motor neuron, an inhibitoryfiber of one nerve cell has a synapse on an excitatory axon of another neuron before the latter communicateswith the motor neuron; in postsynaptic inhibition (top left), the inhibitory and excitatory fibers both synapsedirectly with the target neuron.
A, B, and C illustrate the changes in potential at the excitatory terminal andin the motor neuron when only the excitatory, only the inhibitory, or both inhibitory and excitatory fibers fire.A′, B′, and C′ illustrate membrane potential changes in the motor neuron when only excitatory, only inhibitory, or both excitatory and inhibitory fibers fire.■■A single, large channel for Na+ and K+ carries the chargeduring an endplate potential.
Multiple ion channels areinvolved in a neuronal action potential, which is mainlyproduced by Na+ influx.Repolarization of the endplate is passive, whereasincreased K+ conductance is responsible for repolarization during a neuronal action potential.SKELETAL MUSCLE ORGANIZATIONSkeletal muscle contraction is the basis for voluntary musclemovement. Multinucleated cells contain sarcomeres, specialized structures that produce contraction upon stimulation ofthe muscle. Sarcomeres are contained within myofibrils,which are further organized as muscle fibers; groups of musclefibers form muscle fascicles (Fig. 3.11).
Microscopically, thearrangement of sarcomeres and myofibrils results in the striated appearance of skeletal muscle. Contraction is based onsliding of the thin and thick filaments of sarcomeres (see“Excitation-Contraction Coupling”).Within the skeletal muscle cell, the sarcoplasmic reticulumcomposes a complex network surrounding the myofibrils (Fig.3.12). This specialized form of smooth endoplasmic reticulumis the site for the storage of high concentrations of intracellularCa2+ and contains Ca2+-ATPase and calsequestrin (a lowaffinity Ca2+-binding protein) for sequestration of this ion, as38The Nervous System and MuscleMyelin sheathMitochondriaNeurilemmaActive zoneAxoplasmSchwann cell processSchwann cellAcetylcholine receptor sitesBasement membraneNucleus of Schwann cellPresynaptic membraneActive zoneSynaptic vesiclesSynaptic troughBasement membraneSarcolemmaNucleus of muscle cellMyofibrilsSynaptic cleftPostsynaptic membraneJunctional foldSarcoplasmAcetylcholine receptor sitesFigure 3.10 Structure of the Neuromuscular Junction At the neuromuscular junction, the axonof a motor nerve synapses with skeletal muscle at a site known as the motor endplate.
Stimulation of amotor nerve results in the release of acetylcholine from vesicles at the presynaptic membrane; acetylcholinediffuses and binds to postsynaptic receptors, producing depolarization of the sarcolemma and leading toan action potential.well as L-type (ligand-gated) Ca2+ channels. The transversetubules (T-tubules) are deep invaginations of the muscle cellmembrane (sarcolemma). They form triads with two terminalcisternae of the sarcoplasmic reticulum; these triads arearranged perpendicularly to the muscle fiber.
The T-tubulesextend into the muscle fiber from the surface, allowing closecommunication between the interior of the cell and the extracellular fluid. They are responsible for conducting the actionpotential to the cisternae of the sarcoplasmic reticulum.the gap between the cisternae of the sarcoplasmic reticulumand the T-tubules. Conformational change of the dihydropyridine receptors is believed to produce a subsequent conformational change in the ryanodine receptors, allowingstored Ca2+ to be released from the sarcoplasmic reticulum,initiating the contraction process.
The term excitationcontraction coupling refers to this linking of depolarizationto Ca2+ release.To summarize these events:EXCITATION-CONTRACTION COUPLINGAs depolarization spreads across the sarcoplasmic reticulum,it is conducted into the transverse tubules (Fig. 3.13). The Ttubule membrane contains voltage-gated Ca2+ channels, alsoknown as dihydropyridine receptors. Although the dihydropyridine receptor is a voltage-gated Ca2+ channel, ion fluxthrough this channel is not required for contraction of skeletalmuscle. Rather, a conformational change in the dihydropyridine receptor, caused by depolarization of the T-tubule, isrequired. These receptors are in close apposition to calciumchannel proteins known as ryanodine receptors, which arelarge proteins of the sarcoplasmic reticulum that extend into■■■■■■Depolarization of the motor neuron terminal results inCa2+ influx.Vesicles of the axon terminal release acetylcholine.Binding of acetylcholine by nicotinic receptors results inan endplate potential.An action potential is initiated and is propagated alongthe sarcolemma and down the T-tubules.A conformational change in the dihydropyridine receptor of the T-tubule is transduced to a conformationalchange in the ryanodine receptor of the sarcoplasmicreticulum.Ca2+ is released from the sarcoplasmic reticulum, initiating contraction.Nerve and Muscle PhysiologyCLINICAL CORRELATEMyasthenia GravisMyasthenia gravis is an autoimmune, neuromuscular disease thataffects the acetylcholine receptors of the neuromuscular junction.In this disease, autoantibodies are produced that block or damagethe acetylcholine receptor of the motor endplate, inhibiting thenormal effects of acetylcholine at these receptors and thus producing muscle weakness.
Muscles of the eye and face and musclesinvolved in swallowing, talking, and chewing are most commonlyaffected, although weakness of other muscles may also occur.Episodes of myasthenia gravis may occur suddenly, often after aperiod of high physical activity, and may abate after a period of39rest. A myasthenic crisis is a medical emergency that may becaused by an infectious disease or adverse drug reaction. In acrisis, muscles of respiration are weakened, making breathing difficult.
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