Download Muscle

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Introduction (muscle cell = muscle fibers)
o Myoblasts – stem cells that produce different lines of muscle tissue (embryonic = mesoderm)
 Lack myofilaments, but contain polysomes used to synthesize them
 ALL muscle cells surrounded by an external (basal) lamina
 Fates:
 Skeletal muscle cells
o Fusion of 2 or more myoblastslg multinucleated, cylindrical
o Striated; Somatic (voluntary) division of nervous system
o Satellite cells – undifferentiated cells
 b/w PM & external lamina
 limited skeletal muscle regeneration
 Cardiac muscle cells
o Mesenchyme – mesodermal cells forming embryonic CT; give
rise to cardiac muscle cells
o Mono- or binucleate, striated & branched muscle cells
o Autorhythmic modulated by sympathetic & parasympathetic
o Very limited regeneration
o Intercalated disks
 Smooth muscle cells
o Centrally-placed nucleus
o Mesenchymal myoblasts also form mononucleate smooth mm
o Nonstriated, mononucleate, spindle-shaped (fusiform) cells
o Usually in sheets around tubular organs
o Capable of moderate regeneration
Skeletal Muscle
o Organization: // arrays of actin + myosin  repeating subunits, sarcomeres  long
tubular, striated elements, myofibrils  long, striated, cylindrical, multinucleated muscle
fibers/muscle cells (endomysium & ext. lamina)  fascicles (perimysium)  gross
muscle (epimysium)
 Epimysium: thick, irregular DCT covering the gross muscle
 Perimysium: septae of collagenous CT that wall off bundles (fascicles) of
muscle cells
 Endomysium: highly vascularized, LCT matrix of Type I & III (reticular)
collagen that surrounds individual muscle cells.
 Satellite cells – interior to ext. lamina & external to PM (sarcolemma)
 Can become mitotic
 Limited mm repair
o Structure:
 Understand figure 11.4
 Sarcomere: the morphological & fxn’l unit of contraction in muscle
 Z-line to Z-line; dark line (end of one actin to end of other actin);
length Δ’s
o 2 x ½ I-bands: lightly stained (end of one myosin of 1st
sarcomere to end of another myosin of next sarcomere); length
Δ’s
 A-bands: dark stained (end of one myosin to end of other myosin);
length ≠Δ
o H-band: center where actin does not overlap with myosin
 M-Line: center of sarcomere; myosin anchored to it
 Desmin & Vimentin: intermediate filaments which link adjacent
myofibrils together
 Actin filaments:
 Twisted array of globular actin monomers, tropomyosin & troponin
 Actin to Z-line anchored by α-actin; extend into A-band
 Nebulin: regulate actin filament length
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Myosin filament bundles:
 Thick; across A-band
 Myosin molecules arranged in bundles
o 2 heavy chains consisting of:
 rod-like backbone of helical chains
 2 globular heads w/ ATP binding site & ATPase
o 2 light chains
o Symmetrical around M-Line w/ backbone twd M-Line
o Titin: b/w Z & M-Lines; centers myosin in the sarcromere
 Myomesin – anchors myosin to center of sarcomere at M-Line
 Pure actin & myosin molecules will combine spontaneously
o Contraction:
 B/w myofibrils
 Energy: mitochondria (ATP) & glycogen (Glu storage); backup =
hydrolysis of phosphocreatine
 Regulation of contraction by [Ca2+]: sER (sarcoplasmic reticulum);
sequesters Ca2+ via calsequestrin (Ca2+ binding protein)
 T-tubules: run transversely to myofibrils at A/I band jxns
 Continuation of PM that conducts axn potential into depths of mm cells
 Contraction
 “Uniform” contraction by:
o signal conducts quickly along length of muscle
o T-tubules conduct through depth of muscle cells (voltagesensitive receptors)
 Electrical activity opens voltage-gated receptor to open Ca2+ channels
in sarcoplasmic reticulum
 Influx of Ca2+ into cytoplasm
 Ca2+ binds to troponin & begin the cycle of contraction/”power stroke”
 Power Stroke
o Troponin – Ca2+ and tropomyosin binding domains (TnC/TnT)
o Troponin binds Ca2+ causing conformational Δ in actintropomyosin complex revealing the myosin binding site
o Myosin globular head binds to actin & rotates (“powerstroke”)
to move the actin relative to the myosin
o Actin filaments & attached Z-line are effectively moved
toward the M-line, thus the I-band & sarcomere shortens
o Muscle contracts b/c process is simultaneous in all sarcomeres
 Ca2+-ATPase membrane proteins – pump Ca2+ back into sarcoplasmic
reticulum
 Clinical Correlation:
 Dystrophin – spectrin-like actin binding protein; anchors actin to PM
 Dystrophinlaminincollagenous CT of tendonbone periosteum
(sharpey’s fibers)
 Muscular Dystrophy: defect or absence in dystrophin  progressive
weakening of skeletal muscles
 Rigor Mortis: ATP is required to break the interaction b/w the actin &
myosin; lack of ATP is t/f the basis for the stiffening of muscles
Cardiac Muscle – RAN OUT OF TIME & COULDN’T FINISH
Smooth Muscle – RAN OUT OF TIME & COULDN’T FINISH
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SUMMARY
Nuclei
Location
Striated?
Shape
Axon contact?
Conscious control
Autonomic control
T-tubule location
Myofibrils?
External lamina?
Anchored by
Tissue Coverings
SKELETAL
Many
Peripheral
Yes
Cylinder
All
Yes
No
A/I
Yes
Yes
Endomysium
Epimysium
Perimysium
Endomysium
CARDIAC
1–2
Central
Yes
Branched
Purkinje fibers
No
Yes
Z
Yes
Yes
Intercalated disc
Epicardium
Endocardium
SMOOTH
1
Central
No
Spindle
Some
No
Yes
?
No
Yes
CT
CT