Lecture 6 - Muscle Tissue Flashcards
muscle tissue - cellular features, organization, what are cells specialized for, what is abundant and staining
what is a sarcoplasm, sarcolemma, sarcoplasmic reticulum, muscle fiber, myofilament
- highly cellular tissue- mostly ‘muscle cells’ with some connective tissue
- organized as parallel arrays of elongate cells (bundles)
- cells specialized for contraction and force generation
- abundant actin & myosin cytoskeletal filaments – very
eosinophilic cytoplasm
Special Terms: - sarcoplasm = cytoplasm of muscle cell
- sarcolemma = plasma membrane of muscle cell (and
overlying CT) - sarcoplasmic reticulum = modified smooth ER of muscle
cell - muscle fibre = muscle cell
- myofilament = contractile cytoskeleton
types of muscle tissue and what they do, voluntary or involuntary and strength
Skeletal Muscle
* moves the skeleton (exceptions– tongue, extra-ocular muscles)
* fastest, strongest contraction,
voluntary (reflexes)
Cardiac Muscle
* major component of heart
* rhythmic squeezing continuous & involuntary
Smooth Muscle
* hollow organs (viscera)
* controls diameter
* slowest & weakest contraction,
involuntary
skeletal muscle general features - how long can they be, what do the nuclei look like, what special appearance do they have and what type of sectioning can you see it in
- skeletal muscle fibres can be
several cm long, up to 100 μm in diameter - multi-nucleated with nuclei
pushed to periphery of cell by extensive myofilaments - striations (organized striped
appearance) only obvious in long
skeletal muscle organization -
- actin (thin) & myosin (thick)
filaments (myofilaments) organized into sarcomeres that
repeat end to end - each array of sarcomeres running length of cell is a myofibril
- multiple parallel myofibrils fill
cytoplasm of muscle fibre - multiple muscle fibres bundled
together in a fascicle - multiple muscle fascicles
compose the actual ‘muscle’
thin and thick filaments - what do each of them bind, what do troponin and tropomyosin do
- thick myosin filaments bind ATP
and actin - troponin & tropomyosin cover myosin binding site on actin
- troponin complex binds Ca 2+; changes shape for myosin binding
- thin actin filaments bind myosin
heads
myofilaments in a sarcomere - what are the 3 components in a long section and what they are made of, what extra parts can you see in TEM
- in long section:
-I-band (isotrophic band): thin filaments and associated proteins
from adjacent sarcomeres
-A-band (anisotrophic band): thick
filaments and overlapping portions of thin filaments
-Z-line/disc: primarily desmin; anchors thin filaments from adjacent sarcomeres - in TEM, can also see:
-H-band/zone: central region of A-band that is only myosin thick
filaments
-M-line: myosin anchoring proteins in middle of A-band
muscle contraction - what happens to the sarcomere during contraction
- when muscle contracts each sarcomere shortens as thin filaments slide towards middle: myosin heads bind to actin when Ca2+ present
- Z-lines get closer, I-bands narrow, H-band disappears, no change in A-band or M-line
source of calcium - what is the structure called and what does it consist of, what do they carry, how do they run and what is formed, what does depolarization of them cause
- T-tubules consist of invaginations from sarcolemma
that travel deep into cells along
A-band/I-band in myofibrils - carry membrane depolarization
deep into each fiber - run in proximity to each pair of
SR cisternae to form a Triad - depolarization of T-tubules
causes release of Ca 2+ from SR
network into sarcoplasm in vicinity of myosin heads (i.e. A-Band)
release of calcium - what are the two steps included, what happens for musclule relaxation, what cant myosin heads do
1) input from nervous system
(release of acetylcholine from neuron) leads to depolarization of sarcolemma via ACh receptors on muscle
2) wave of depolarization travels down T-tubules and leads to opening of voltage gated Ca 2+ channels on SR
* Ca 2+ floods sarcoplasm,
leading to sliding of filaments
and sarcomere shortening
Muscle Relaxation: release of Ca 2+ also triggers activity of Ca ++-
activated ATPase to pump Ca 2+ back into SR
* myosin heads can’t bind actin; thin filaments slide back to resting state
powering the system - what is essential for muscle contraction and why, how is it generated
ATP is essential for muscle contraction:
* to allow myosin heads to bind and flex
* to power ion pumps (in SR, T-tubules and sarcolemma) to
restore resting state ATP is generated from glycogen stores by mitochondria
controlling the system - what does every skeletal muscle fiber have, what is a motor unit made of, what does the AP in that neuron lead to
- every skeletal muscle fibre (cell) has direct neural input at motor end plate (MEP)
- each motor neuron can provide a MEP to just a few (or even a single) or up to over 100 muscle fibres = Motor Unit
- action potential in that neuron leads to all or none contraction of every fibre in that Motor Unit
muscle organization - what is each skeletal muscle fiber surrounded by and what does that consist of, what are the fascicles covered by, what are bundles of fascicles covered by, where are blood vessels and nerves
- each skeletal muscle fibre is
surrounded by endomysium,
consisting of a basal lamina - fascicles of muscle fibres are
surrounded by thicker CT layer of
perimysium; muscle fibres within the perimysium comprise a motor unit - bundles of fascicles are enveloped by a tough dense CT epimysium
- blood vessels and nerves penetrate these CT layers to travel to surface of individual muscle fibres
skeletal muscle force transmission - what is the epimysium containuous with and what does it merge into, what does muscle contraction allow, how is force of sarcomere shortening transmitted, what connects actin myofilaments to ECM, what is sarcoplasmic contractile activity linked to, what does the number of engaged motor units determine
- the epimysium is continuous
with the muscle fascia and the muscle tendon, which merge with periosteum - muscle contraction allows
body movement because muscles are anchored to bone by CT - sarcoplasmic contractile activity is thus linked to the CT sheaths and hence to bone
- number of Motor Units engaged determines nature of the ‘muscle’
contraction: course vs fine movement, weak vs strong contraction
general features of cardiac muscle - size of special cells compared to skeletal, nucleus appearance, what is prominent, what specialized junctions are there and what do they do, what are chains of cardiac muscle covered by, where is this found
- striated cells much smaller than skeletal muscle fibres
- branched shape with centrally located nucleus; sometimes bi-nucleate
- prominent glycogen pool often seen in perinuclear region
- specialized junctions (intercalated discs) hold cells together end to end in linear chains
- chains of cardiac muscle covered by endomysium and irregular bundles covered by
perimysium - cardiac muscle found in heart and large veins close to heart
intercalated discs - what do parts of junctions do they have, what three things are included and what they do
- Intercalated Discs have Transverse (end to end) and Longitudinal parts of junctions:
Fascia adherens (≅ zonula adherens; transverse region) - connects and anchors actin filaments to sarcolemma Macula adherens (= desmosomes; transverse & longitudinal regions)
- interconnects intermediate filaments & hold cells together
Gap Junctions (longitudinal regions) - transmembrane protein pores that couple cytoplasm of adjacent cells
cardiac muscle cell ultrastructure - how are the myofilaments organized compared to skeletal, T tubules size and where they run along, what is specific to this type
- myofilaments organized into sarcomeres same as for skeletal muscle
- T-tubules much larger diameter and run along Z-lines of sarcomeres
- SR network and cisternae are far less developed than in skeletal muscle; seen as membrane profile with T-tubule and called a Diad
cardiac muscle cell contraction - neuronal input, what triggers depolarization, how long does the wave last and what does it open, what happens after that, is contraction faster or slower than skeletal
Similar but not identical to contraction of skeletal muscle:
* no individual neural input to each cardiac muscle
* depolarization is triggered by specialized cardiac conduction
cells and/or spreads from cell to cell via gap junctions in intercalated disc
* wave of depolarization is longer lasting and leads to opening of
voltage gated Ca2+ channels on T-tubule
* Ca2+ enters sarcoplasm from lumen of T-tubule (i.e. from outside of cell)
* presence of Ca2+ triggers additional Ca2+ release into
sarcoplasm
Hence: cardiac muscle contraction is slower and bundles of fibres contract in coordinated fashion
powering cardiac muscle - what is essential and why, how is it generated and what is numerous here
ATP is also essential for cardiac muscle contraction:
* to allow myosin heads to bind and flex
* to power ion pumps (in SR and T-tubules) to restore resting state
* ATP is generated from glycogen stores (green arrows) and especially from lipid stores (blue arrows)
* mitochondria numerous and very large in cardiac muscle cells
smooth muscle general features - nucleus, striations, how are they found and where, what are they similar to
-fusiform cells with abundant
cytoplasm and single central nucleus; no striations
* usually found in large bundles
* walls of blood vessels & viscera
* superficially similar to fibroblasts but plumper nucleus; more obvious cytoplasm
smooth muscle arrangements - in tubular viscera vs spherical viscera, whatt does contraction do in each
- in tubular viscera (e.g. intestine)
arranged as inner circular
(circumferential) and outer
longitudinal bundles/multiple
layers of smooth muscle cells - contraction often reduces diameter of tube
- in spherical viscera (e.g. urinary
bladder) arranged as multiple bundles of smooth muscle cells oriented in different directions - contraction causes size of sphere to contract in all directions
smooth muscle ultrastructure - what do the cells contain, how does cell contraction happen and what is not obvious, what are myofilaments anchored to
- smooth muscle cells contain actin and myosin contractile filaments, but in much lower amounts than skeletal and cardiac muscle
- use similar sliding filament mechanism to cause cell contraction, but no obvious sarcomere arrangement
- myofilaments are anchored to dense bodies (somewhat equivalent to Z-lines), which are connected together in a network by intermediate filaments, and anchored to sarcolemma at attachment plaques
smooth muscle contraction - how does myosin head move along, what does it interact with, what happens when filament slides
- in smooth muscle thick filament,
myosin heads project all along
filament length - interact with actin thin filaments
anchored to dense bodies &
attachment plaques - when filaments slide, pull dense
bodies closer together; pull edges of cell closer together
smooth muscle contraction control - what dont they have compared to the other muscle types, what increases surface area slightly, how does calcium enter, what does it still require but how does binding protein work, what binds actin
- no organized T-tubules; calveolae increase cell surface area slightly; no extensive SR network
- Ca 2+ released from SR via 2nd messenger signalling system; Ca 2+ also enters cell from exterior
- still require ATP and Ca 2+, but Ca 2+ binding protein (calmodulin) acts with myosin light chain kinase (MLCK) to phosphorylate myosin head
- phosphorylated myosin binds actin, etc
smooth muscle contraction control - variety of what, is every cell innervated, neurotransmitters and their effect, what propogates signal and what does it form, how is force of contraction transmitted, slow or fast process, examples of when contraction happens
- variety of signals for entry of Ca2+ from outside cell – nervous,
hormonal, stretch, etc. - not every cell is innervated & not by typical neuromuscular
junctions - variety of neurotransmitters (not just ACh), some of which are
inhibitory - gap junctions between smooth muscle cells propagate the signal & form functional syncitium
- force of contraction is transmitted via collagen fibers of ECM
in endomysium and perimysium - smooth muscle contraction is slower process – slower reaction time and slower contraction time
- contraction can be very sustained (many minutes): cramping, peristalsis, vascular tone, etc.
muscle repair and regeneration - in all three muscle types, hyperplasia, belgian blue cattle
Skeletal Muscle
* fibres form during development by fusion of precursor cells
* satellite cells remain associated
with differentiated fibres in adult tissue
* act as cellular reserve for muscle repair: proliferate & differentiate into myoblasts then fuse to form myofibres
Cardiac Muscle
* no satellite cells but possibly small reserve of stem cells that can proliferate
Smooth Muscle
* no satellite cells but smooth muscle cells seem capable of considerable proliferation in response to stretch, hormones, etc
- in addition to variable cell proliferation (hyperplasia), muscle can also undergo hypertrophy: increase in muscle mass without cell proliferation
- increase in both amount of myofibrils and in amount of SR within an individual cell- increased diameter and mass of cell
- common in skeletal and cardiac muscle when increased load (exercise)
Belgian Blue cattle
* Myostatin mutation leads to excess myoblast formation during development
* animals have excessive muscle mass due to # of fibres, not due to increased fibre size
* some evidence that exogenous testosterone enhances # of stem cells
