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PowerPointPowerPoint®® Lecture Slides prepared by Lecture Slides prepared byStephen Gehnrich, Salisbury UniversityStephen Gehnrich, Salisbury University
5C H A P T E R
Cellular Movement Cellular Movement and Muscles (2)and Muscles (2)
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Muscle Cells (Myocytes)
Myocytes (muscle cells) Contractile cell unique to animals
Contractile elements within myocytes Thick filaments
Polymers of myosin ~300 myosin II hexamers
Thin filaments Polymers of -actin Ends capped by tropomodulin and CapZ to stabilize Proteins troponin and tropomyosin on outer surface
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Thick and Thin Filaments
Figure 5.15
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Muscle Cells
Two main types of muscle cells are based on the arrangement of actin and myosin Striated (striped appearance)
Skeletal and cardiac muscle Actin and myosin arranged in parallel
Smooth (do not appear striped) Actin and myosin are not arranged in any particular way
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Striated and Smooth Muscle
Figure 5.16
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Striated Muscle Types
Table 5.3
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Striated Muscle Cell Structure
Thick and thin filaments arranged into sarcomeres Repeated in parallel and in series
Side-by-side across myocyte Causes striated appearance
End-to-end along myocyte
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Sarcomeres
Structural features of sarcomeres Z-disk
Forms border of each sarcomere Thin filaments are attached to the Z-disk and extend from
it towards the middle of the sarcomere
A-band (anisotropic band) Middle region of sarcomere occupied by thick filaments
I-band (isotropic band) Located on either side of Z-disk Occupied by thin filament
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Sarcomeres
Thin and thick filaments overlap in two regions of each sarcomere
Each thick filament is surrounded by six thin filaments
Three-dimensional organization of thin and thick filaments is maintained by other proteins Nebulin
Along length of thin filament
Titin Keeps thick filament centered in sarcomere Attaches thick filament to Z-disk
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Sarcomeres
Figure 5.17
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Three-Dimensional Structure of Sarcomere
Figure 5.18
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Muscle Actinomyosin Activity is Unique
Myosin II cannot drift away from actin Structure of sarcomere
Duty cycle of myosin II is 0.05 (not 0.5) Each head is attached for a short time Does not impede other myosins from pulling the thin
filament
Unitary displacement is short Small amount of filament sliding with each movement
of the myosin head
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Myofibril
In muscle cells, sarcomeres are arranged into myofibrils Single, linear continuous stretch of interconnected
sarcomeres (i.e., in series) Extends the length of the muscle cell Have parallel arrangement in the cell
More myofibrils in parallel can generate more force
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Myofibrils in Muscle Cells
Figure 5.20
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Regulation of Contraction
Excitation-contraction coupling (EC coupling) Depolarization of the muscle plasma membrane
(sarcolemma) Elevation of intracellular Ca2+
Contraction Sliding filaments
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Ca2+ Allows Myosin to Bind to Actin
At rest, cytoplasmic [Ca2+] is low Troponin-tropomyosin cover myosin binding sites on
actin
As cytoplasmic [Ca2+] increases Ca2+ binds to TnC (calcium binding site on troponin) Troponin-tropomyosin moves, exposing myosin-
binding site on actin Myosin binds to actin and cross-bridge cycle begins Cycles continue as long as Ca2+ is present Cell relaxes when the sarcolemma repolarizes and
intracellular Ca2+ returns to resting levels
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Troponin and Tropomyosin
Figure 5.21
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Regulation of Contraction by Ca2+
Figure 5.22
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Ionic Events in Muscle Contraction
Figure 5.23
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Troponin–Tropomyosin Isoforms
Properties of isoforms affect contraction For example, fTnC has a higher affinity for Ca2+ than
s/cTnC Muscle cells with the fTnC isoform respond to smaller
increases in cytoplasmic [Ca2+]
Isoforms differ in the affect of temperature and pH
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Myosin Isoforms
Properties of isoforms affect contraction Multiple isoforms of myosin II in muscle Isoforms can change over time
Table 5.4
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Excitation of Vertebrate Striated Muscle
Skeletal muscle and cardiac muscle differ in mechanism of excitation and EC coupling
Differences include Initial cause of depolarization Time course of the change in membrane potential
(action potential) Propagation of the action potential along the
sarcolemma Cellular origins of Ca2+
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Action Potentials
APs along sarcolemma signal contraction Na+ enters cell when Na+ channels open
Depolarization
Voltage-gated Ca2+ channel open Increase in cytoplasmic [Ca2+]
Na+ channels close K+ leave cell when K+ channels open
Repolarization
Reestablishment of ion gradients by Na+/K+ ATPase and Ca2+ ATPase
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Time Course of Depolarization
Figure 5.24
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Initial Cause of Depolarization
Myogenic (“beginning in the muscle”) Spontaneous
For example, vertebrate heart
Pacemaker cells Cells that depolarize fastest Unstable resting membrane potential
Meurogenic (“beginning in the nerve”) Excited by neurotransmitters from motor nerves
For example, vertebrate skeletal muscle
Can have multiple (tonic) or single (twitch) innervation sites
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Neurogenic Muscle
Figure 5.25
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T-Tubules and Sarcoplasmic Reticulum
Transverse tubules (T-tubules) Invaginations of sarcolemma Enhance penetration of action potential into myocyte More developed in larger, faster twitching muscles Less developed in cardiac muscle
Sarcoplasmic reticulum (SR) Stores Ca2+ bound to protein sequestrin Terminal cisternae increase storage
T-tubules and terminal cisternae are adjacent to one another
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T-Tubules and SR
Figure 5.28
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Ca2+ Channels and Transporters
Channels allow Ca2+ to enter cytoplasm Ca2+ channels in cell membrane
Dihydropyridine receptor (DHPR)
Ca2+ channels in the SR membrane Ryanodine receptor (RyR)
Transporters remove Ca2+ from cytoplasm Ca2+ transporters in cell membrane
Ca2+ ATPase Na+/Ca2+ exchanger (NaCaX)
Ca2+ transporters in SR membrane Ca2+ ATPase (SERCA)
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Ca2+ Channels and Transporters
Figure 5.27
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Induction of Ca2+ Release From SR
AP along sarcolemma conducted down T-tubules Depolarization opens DHPR Ca2+ enters cell from extracellular fluid
In heart, [Ca2+] causes RyR to open, allowing release of Ca2+ from SR “Ca2+ induced Ca2+ release”
In skeletal muscle, change in DHPR shape causes RyR to open, allowing release of Ca2+ from SR “Depolarization induced Ca2+ release”
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Ca2+ Induced Ca2+ Release
Figure 5.29
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Depolarization Induced Ca2+ Release
Figure 5.30
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Relaxation
Repolarization of sarcolemma Remove Ca2+ from cytoplasm
Ca2+ ATPase in sarcolemma and SR Na+/Ca2+ exchanger (NaCaX) in sarcolemma Parvalbumin
Cytosolic Ca2+ binding protein buffers Ca2+
Ca2+ dissociates from troponin Tropomyosin blocks myosin binding sites Myosin can no longer bind to actin
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Relaxation
Figure 5.27
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Summary of Striated Muscles
Table 5.5