Cellular Movement and Muscles (2)

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5C H A P T E R

Cellular Movement Cellular Movement and Muscles (2)and Muscles (2)


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


Thick and Thin Filaments

Figure 5.15


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


Striated and Smooth Muscle

Figure 5.16


Striated Muscle Types

Table 5.3


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


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


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


Sarcomeres

Figure 5.17


Three-Dimensional Structure of Sarcomere

Figure 5.18


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


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


Myofibrils in Muscle Cells

Figure 5.20


Regulation of Contraction

Excitation-contraction coupling (EC coupling) Depolarization of the muscle plasma membrane

(sarcolemma) Elevation of intracellular Ca2+

Contraction Sliding filaments


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


Troponin and Tropomyosin

Figure 5.21


Regulation of Contraction by Ca2+

Figure 5.22


Ionic Events in Muscle Contraction

Figure 5.23


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


Myosin Isoforms

Properties of isoforms affect contraction Multiple isoforms of myosin II in muscle Isoforms can change over time

Table 5.4


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+


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


Time Course of Depolarization

Figure 5.24


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


Neurogenic Muscle

Figure 5.25


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


T-Tubules and SR

Figure 5.28


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)


Ca2+ Channels and Transporters

Figure 5.27


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”


Ca2+ Induced Ca2+ Release

Figure 5.29


Depolarization Induced Ca2+ Release

Figure 5.30


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


Relaxation

Figure 5.27


Summary of Striated Muscles

Table 5.5

Cellular Movement and Muscles (2)

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