chapter 11– muscular tissue
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Chapter 11– Muscular Tissue. 11- 1. Ch. 11 Study Guide. Critically read Chapter 11 pp. 402-418 before 11.5 section (Behavior of whole muscles) Comprehend Terminology (those in bold in the textbook) within the reading scope above - PowerPoint PPT PresentationTRANSCRIPT
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CHAPTER 11– MUSCULAR TISSUE
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Ch. 11 Study Guide 1. Critically read Chapter 11 pp. 402-418 before
11.5 section (Behavior of whole muscles)2. Comprehend Terminology (those in bold in the
textbook) within the reading scope above3. Study-- Figure questions, Think About It
questions, and Before You Go On (section-ending) questions (within the reading scope above)
4. Do end-of-chapter questions—– Testing Your Recall— 1-5, 7, 13-16– True or False– 1-2, 4-5
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§ 11.0-- Introduction to Muscle
• Movement is a fundamental characteristic of all living things
• In animals, muscular tissues capable of shortening– How (molecular mechanism)?
• Three types of muscle tissue--
• Focuses of this chapter– structure, contraction, and metabolism of skeletal muscle at the cellular/molecular levels
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§ 11.1--Characteristics of ALL Muscle CellsChanges--•Responsiveness (excitability)
– Respond to stimuli with electrical changes; in what cells?•Conductivity
– 2 Purposes– more than a local electrical change; leading to muscle contraction
Consequences– of muscles•Contractility –shortens when stimulated; pull on bones and other tissues•Extensibility -- capable of being stretched; in other cells— What happen?
•Elasticity -- returns to its original resting length after being stretched
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§ Skeletal Muscle
• Def. -- Voluntary striated muscle usually attached to bones
Explanation--
• Striations -- (Fig. 11.1)– What are they?
• Voluntary – why? Under conscious control
• A typical skeletal muscle cell/muscle fiber– length: 3-30 cm long; 100 micrometer in diameter
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Figure 11.1
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(cell)
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Connective Tissue--• C.T. attachments between muscle and bone
– Endomysium (surrounds each muscle fiber), – ___________ ( . . . fascicle)– ___________ (. . . whole muscle; grades into fascia
(CT sheet))– to bones (may/may not via tendon)
• Collagen fibers (include those structures listed above) are extensible and elastic– stretches slightly and recoils when released– Advantage of stretching– protect m. from injury;
recoiling of m. help to return to resting length
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§ 11.2 Microscopic Anatomy Of Skeletal Muscle– Key words:Multinucleate, Striations, Voluntary
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Fig. 11.2– ONE skeletal muscle fiber-- A (#1)
B--Myofibrils (protein bundles)
C--3 types of myofilaments (proteins)
SR
T-tubule
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A. Muscle fiber – one skeletal muscle cellB. Myofibril –forming an internal
subdivision of a cardiac or skeletal muscle cell
C. Myofilament – a protein microfilament responsible for the contraction of a muscle cell; – 3 kinds— ??
§ Skeletal muscle fiber (#2)
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• Sarcoplasm (cytoplasm) is filled with – Myofibrils– Glycogen– purpose?– Pigment (myoglobin)—binding oxygen
• Sarcoplasmic reticulum = smooth ER– network around each myofibril; function? Store
calcium– terminal cisternae–– triad =
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§ Skeletal muscle fiber (#3)
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Skeletal Muscle Fibers #4• Multiple flattened nuclei inside cell membrane
– fusion of multiple myoblasts during development
• Sarcolemma – plasma membrane; having tubular infoldings (transverse (T) tubules) that penetrate the interior of the cell– carry electric current to interior of the cell– This current signals the SR when to release calcium
ions into cytoplasm
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§ Three kinds of myofilament – 1. Thick Filaments
• Each thick filament is made of 200 to 500 ________ molecules– each in turn has– 2 entwined polypeptides (the heads similar to golf clubs)
for each myosin molecule
• Arranged in a bundle of “golf clubs” with heads directed outward in a spiral array around the bundled tails
• Central area of the thick filament is a _________ with no heads (of myosin molecules)
Fig. 11.3 a, b, d 11-13
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SINGLE MYOSIN MOLECULE
Myosin molecules to form thick filament—see next slide
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(partial view)
Full picture of the thick filament—see next slide
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Overlap of Thick and Thin Filaments
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Three kinds of myofilament – 2. Thin Filaments (Fig. 11.3c)
• (in red) 2 intertwined strands (fibrous (F) actin) – Each bead is a globular (G) actin with an active site;
capable of binding the head of a __________
• (in white) Groove holds ____________ molecules– each can block 6 or 7 active sites of G actins
• (in yellow) calcium-binding _________ molecule on each tropomyosin molecule
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A blow-up image in the next slide
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Two interwined chains (F actins; in red) are shown.
F actin
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• Springy proteins called ________________
• Anchor each thick filament to Z disc
• Prevents overstretching of sarcomere
Fig. 11.5
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Three kinds of myofilament – 3. Elastic Filaments (Fig. 11.5)
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SarcomereI band I band A band
H band
Thick filamentTitinThin filament
Elastic filament(b)
Z discZ discM line
3 kinds of myofilament in three colors—Purple ones— _____________ filamentsRed ones— ____________ filamentsGreen ones-- _____________ filaments
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§ Contractile & Regulatory Proteins• Myosin and actin are
contractile proteins; do the work of shortening the muscle fiber
• ________________ and _____________ are regulatory proteins; Function--
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§ Striations = Organization of Filaments• Striations-- Dark A bands alternating with lighter I
bands
• A band is thick filament region— Dark/Light (Circle one)– central H band area is lighter, contains no thin filaments
• I band is thin filament region— Dark/Light (Circle one)– bisected by Z disc protein, anchoring elastic and thin filaments– from one Z disc (Z line) to the next is a sarcomere (Fig. 11.5)
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SARCOMERE– contractile unit in a striated muscle fiber; extending from one Z disc to the next Z disc
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§ Relaxed & Contracted Sarcomeres
• Muscle cells shorten because their individual Sarco________________ shorten
• Details--– Do myofilaments change length? Yes/No– Z discs/sarcomeres? Yes/No– Eventually pulling on sarcolemma (cell mem.) via
proteins (especially dystrophin) Fig. 11.4
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Exterior of the muscle cell
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§ 11.3--Nerve-Muscle Relationships
• Skeletal muscles are innervated by somatic motor neurons
• Where are motor neurons’ cell bodies? In ____________________________
• Axons reach these muscle fibers– At its distal end, each axon branches about 200 times;
each branch reaches a different fiber (cell)
• Each motor neuron and all the muscle fibers it innervates are called a _______________
Fig. 11.6
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•Motor neuron originated from—
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A
D
CBE F
G
H
A, B, C, D; E, F, G, H
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Motor Units (Fig. 11.7—next slide)
•Def. A motor neuron and the muscle fibers it innervates– A muscle (whole muscle) is innervated by _________ motor
units; advantages?– Where are the muscle fibers innervated by one motor
neuron?
• Small motor units--Fine control– small motor units contain as few as 3-6 muscle fibers per
nerve fiber– Example– eye muscle
• Large motor units--Strength control– gastrocnemius muscle has 1000 fibers per nerve fiber
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§ Neuromuscular Junctions (NMJ)- 1
• Functional connection between nerve fiber and target cell called synapse; if the target cell is a muscle fiber, the synapse is called NMJ
• Neurotransmitter (acetylcholine/ACh) released from nerve fiber stimulates muscle cell
• Components of NMJ– Fig. 11.7 (next slide)– A-synaptic knob (with vesicles present; B)– C-synaptic cleft (a tiny gap)– D-motor end plate– E-junctional folds
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The Neuromuscular Junction- 2
D. Motor end plate
A.
C.
E.
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B.
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§ Neuromuscular Junctions- 3
Components of NMJ:– A) synaptic knob-- a swollen end of a nerve fiber– B) synaptic vesicles-- ________________– C) synaptic cleft-- tiny gap
_________________________________– D) motor end plate— depression region of
sarcolemma where a ______________ rests• Features– increases surface area for Ach receptors and
contains Acetylcholinesterase
– E) junctional folds— infoldings in sarcolemma; many Ach receptors present here too
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Neuromuscular Toxins on Muscle:1. Spastic paralysis (& possible suffocation)
– Symptom: a continual contraction of the muscle– Caused by pesticides (cholinesterase inhibitors) – Mechanism: binds to acetylcholinesterase and prevents it
from degrading ACh
2. Tetanus (lockjaw) is another spastic paralysis caused by toxin of Clostridium tetani bacteria
– blocks glycine release in the spinal cord and causes overstimulation of the muscles
3. Flaccid paralysis (limp muscles, cannot contract) due to curare that competes with Ach receptor sites
– respiratory arrest (thoracic muscles cannot contract)
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§ Electrically excitable cells1. In what specific cells?
2. At rest, plasma membrane is charged – difference in charge across the membrane = resting membrane
potential (-90 mV in cells)
– Why?
3. Stimulation opens ion gates in membrane– When strong enough, results in action potential production
– Details• Depolarization-- Na+ ion gates open; sodium ions enter
• Repolarization followed-- K+ rushes out of cell
4. An action potential spreads—– Where? Cell surface of nerve fibers/sarcolemma
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§ Muscle Contraction and Relaxation
• Four phases involved in this process– A. excitation = nerve action potentials lead to
action potentials in muscle fiber– B. excitation-contraction coupling =
action potentials on the sarcolemma activate myofilaments
– C. contraction = shortening of muscle fiber – D. relaxation = return to resting length
• Images will be used to demonstrate the steps of each of these actions
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A. Excitation (steps 1-5)– These events link action potentials in the nerve fiber to the generation of action potentials in the muscle fiber.
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• Nerve signal opens voltage-gated Calcium channels. Calcium stimulates exocytosis of synaptic vesicles containing _____; then ACh release into synaptic cleft
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Steps 1-2 of excitation
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Steps 3-4 of excitation
Binding of ACh to receptor proteins opens Na+ and K+ channels resulting in an end-plate potential (EPP), RMP from -90mV to +75mV and back to -90mV 11-38
Na+ goes in first
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Voltage change in end-plate region (EPP) opens nearby voltage-gated channels producing an action potential (cell?)
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Step 5 of excitation
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B. Excitation-Contraction Coupling (steps 6-9)– These events link action potentials in the muscle fiber to the release and binding of calcium ions
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Action potential spreading over sarcolemma and down T-tubules, causing calcium gates to open in SR; Purpose? Calcium enters . . .
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Steps 6-7-- excitation-contraction coupling
Triad?
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• Calcium released by SR binds to ___________• Troponin-tropomyosin complex changes shape and
exposes _____________on actin filaments
Thin Filament
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Steps 8-9-- excitation-contraction coupling
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C. Contraction (steps 10-13)– The sliding filament mechanism of contraction
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Steps 10-11-- Contraction
• Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it into an extended position
• It binds to actin active site forming a cross-bridge 11-44
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Steps 12-13-- Contraction
• Step 13--With the binding of more ATP, the myosin head releases and extends to attach to a new active site
• Step 12--myosin head releases ADP/phosphate as it pulls the thin filament past the thick one
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D. Relaxation of a muscle fiber (steps 14-18)– These events lead from the cessation of a nerve signal to the release of thin filaments by myosin
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Nerve stimulation ceases and acetylcholinesterase removes ACh from receptors. Stimulation of the muscle cell ceases.
Steps 14-15-- Relaxation
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Step 16-- Relaxation• Active transport
needed to pump calcium back into SR (ATP needed)
• Calcium binds to _____________
• ATP is needed for muscle relaxation (as well as muscle contraction)
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Steps 17-18-- Relaxation
Step 17: ATP binding--• Loss of calcium from
sarcoplasm moves troponin-tropomyosin complex over active sites
ATP binding and the cross bridge detaches
Step 18: Muscle fiber returns to resting length
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§ Impact of calcium ions in muscle contraction
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What are shortened during muscle contraction?A band, H-zone, I band, actin, myosin, sarcomeres?
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§ Rigor Mortis (death rigor)
• Symptom: stiffening of the body beginning 3 to 4 hours after death
• Causes: Calcium activates myosin-actin cross-bridging and muscle contracts, but can not relax.
• Mechanisms: muscle relaxation requires ______ and ATP production is no longer produced after death
• Thick and thin filaments remain rigidly cross-linked. Fibers remain contracted until myofilaments decay, proteins break down.
Take home message-- Cross bridge detachment is ATP required
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§ Length-Tension Relationship
Amount of tension generated depends on length of muscle before it was stimulated:– length-tension relationship (see graph next slide)
1. Overly contracted (weak contraction results)– thick filaments too close to Z discs and can’t slide
2. Too stretched (weak contraction results)– little overlap of thin and thick does not allow for very many
cross bridges to form
3. Optimum resting length produces greatest force when muscle contracts– Ex. CNS maintains optimal length producing muscle tone or
partial contraction
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Length-Tension Curve
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