1 II Action Potential Successive Stages: (1)Resting Stage (2)Depolarization stage (3)Repolarization...
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Transcript of 1 II Action Potential Successive Stages: (1)Resting Stage (2)Depolarization stage (3)Repolarization...
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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)
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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
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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.
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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
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MUSCLES-About this Chapter
• Skeletal muscle• Mechanics of body movement• Smooth muscle• Cardiac muscle
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The Three Types of Muscle
Figure 12-1a
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The Three Types of Muscle
Figure 12-1b
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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
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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