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II Action Potential

Successive Stages:

(1) Resting Stage

(2) Depolarization stage

(3) Repolarization stage

(4) After-potential stage

(1)

(2) (3)

(4)

Phases of the Action Potential Are Controlled by Gating Mechanisms of Voltage-Gated Ion Channels-

•The depolarizing and repolarizing phases of the action potential can be explained by relative changes in membrane conductance (permeability) to sodium and potassium.• During the rising phase, the nerve cell membrane becomes more permeable to sodium, as a consequence the membrane potential begins to shift more toward the equilibrium potential for sodium which is ?•(ENa = +60mv). •However, before the membrane potential reaches ENa, sodium permeability begins to decrease and potassium permeability increases. This change in membrane conductance again drives the membrane potential toward EK,-

•Which is?(EK = -97mV), accounting for repolarization of the membrane

Clinical Focus-Channelopathies•Voltage-gated channels for sodium, potassium, calcium, and chloride are intimately associated with excitability in neurons and muscle cells and in synaptic transmission.•Channelopathies affecting neurons include episodic and spinocerebellar ataxias, some forms of epilepsy, and familial hemiplegic migraine. •Ataxias are a disruption in gait mediated by abnormalities in the cerebellum and spinal motor neurons. One specific ataxia associated with an abnormal potassium channel is episodic ataxia with myokymia. In this disease, which is autosomal-dominant, cerebellar neurons have abnormal excitability and motor neurons are chronically hyperexcitable. This hyperexcitability causes indiscriminant firing of motor neurons, observed as the twitching of small groups of muscle fibers, akin to worms crawling under the skin (myokymia).•One of the best-known sets of channelopathies is a group of channel mutations that lead to the Long Q-T (LQT) syndrome in the heart. The QT interval on the electrocardiogram is the time between the beginning of ventricular depolarization and the end of ventricular repolarization. In patients with LQT, the QT interval is abnormally long because of defective membrane repolarization, which can lead to ventricular arrhythmia and sudden death

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Action Potential Summary

Reduction in membrane potential (depolarization) to "threshold" level leads to opening of Na+ channels, allowing Na+ to enter the cell

Interior becomes positive The Na+ channels then close automatically

followed by a period of inactivation. K+ channels open, K+ leaves the cell and the

interior again becomes negative. Process lasts about 1/1000th of a second.

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Properties of the Action Potential “All or none” phenomenon

A threshold or suprathreshold stimulus applied to a single nerve fiber always initiate the same action potential with constant amplitude, time course and propagation velocity.

Propagation Transmitted in both direction in a nerve

fiber

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Positive feedback loop

Reach “threshold”?

If YES, then...

Stimulation

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V. Propagation of the Action Potential

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The Speed of Propagation of the Action Potential Depends on Axon Diameter and MyelinationAfter an action potential is generated, it propagates along the axon toward the axon terminal, it is conducted along the axon with no decrement in amplitude. The mode in which action potentials propagate and the speed with which they are conducted along an axon depend on whether the axon is myelinated. The diameter of the axon also influences the speed of action potential conduction: larger-diameter axons have faster action potential conduction velocities than smaller-diameter axons.

Table 4–1 Nerve Fiber Types in Mammalian Nerve. a

Fiber Type Function Fiber Diameter (m)

Conduction Velocity (m/s)

A alpha Proprioception; somatic motor 12–20 70–120

beta Touch, pressure 5–12 30–70Gamma Motor to muscle spindles 3–6 15–30Delata Pain, cold, touch 2–5 12–30B Preganglionic autonomic <3 3–15C Dorsal root Pain, temperature, some

mechano-reception0.4–1.2 0.5–2

SympatheticPostganglionic sympathetic 0.3–1.3 0.7–2.3

Nerve Fiber Types in Mammalian Nerve

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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.

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Saltatory Conduction

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Slide 3 of 28

MUSCLES-About this Chapter

• Skeletal muscle• Mechanics of body movement• Smooth muscle• Cardiac muscle

The Three Types of Muscle

Figure 12-1a

The Three Types of Muscle

Figure 12-1b

The Three Types of Muscle

Figure 12-1c

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Skeletal Muscle

Human body contains over 400 skeletal muscles40-50% of total body weight

Functions of skeletal muscle-GenratesForce for locomotion and breathingForce production for postural supportHeat production during cold stress

Anatomy Summary: Skeletal Muscle

Figure 12-3a (2 of 2)

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Fascicles: bundles, CT(connective tissue) covering on each one

Muscle fibers: muscle cells

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Structure of Skeletal Muscle:Microstructure

SarcolemmaTransverse (T) tubuleLongitudinal tubule (Sarcoplasmic

reticulum, SR)Myofibrils

Actin (thin filament)TroponinTropomyosin

Myosin (thick filament)

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Within the sarcoplasm

Transverse tubules

Sarcoplasmic reticulum -Storage sites for calcium

Terminal cisternae - Storage sites for calcium

Triad

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Microstructure of Skeletal Muscle (myofibril)

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Sarcomeres Sarcomere : bundle of alternating thick and

thin filaments Sarcomeres join end to end to form myofibrils

Thousands per fiber, depending on length of muscle

Alternating thick and thin filaments create appearance of striations

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Myosin head is hinged Bends and straightens during contraction

Myosin

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Thick filaments (myosin)Bundle of myosin proteins shaped like double-

headed golf clubsMyosin heads have two binding sites

Actin binding site forms cross bridgeNucleotide binding site binds ATP (Myosin ATPase)

Hydrolysis of ATP provides energy to generate power stroke

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Thin filaments

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Thin filaments (actin)Backbone: two strands of polymerized globular

actin – fibrous actinEach actin has myosin binding site

TroponinBinds Ca2+; regulates muscle contraction

TropomyosinLies in groove of actin helixBlocks myosin binding sites in absence of Ca2+

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Thick filament: Myosin (head and tail) Thin filament: Actin, Tropomyosin, Troponin

(calcium binding site)

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III Molecular Mechanism of Muscular Contraction

The sliding filament model Muscle shortening is due to movement of the actin

filament over the myosin filament

Reduces the distance between Z-lines

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The Sliding Filament Model of Muscle Contraction

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Changes in the appearance of a Sarcomere during the Contraction of a Skeletal Muscle Fiber

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Cross-Bridge Formation in Muscle Contraction

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Energy for Muscle Contraction

ATP is required for muscle contractionMyosin ATPase breaks down ATP as fiber

contracts