Contractile Cells, Skeletal, Cardiac, Smooth Flashcards
What is contraction in a muscle cell?
interaction of the proteins
- actin and myosin
fuelled by ATP
driven by a rise in calcium concentration
What are the different parts of the muscle cell? What connects a bone and muscle?
a single muscle cell = muscle fibre/myofibril
a group/bundle of muscle fibres = fasicle
endomysium - tissue surrounding each individual muscle cell
perimysium - tissue surrounding bundle of muscle fibres
epimysium - connective tissue surrounding fascicles (group of muscle cells)
tendon connects a bone and muscle
What are the components of a single muscle cell? How does it contract?
myofibril
- has actin (thin filament) and myosin (thick filament) which are the contractile proteins
- has sarcoplasmic reticulum along the myofibril complex
= is a intracellular store of calcium, is triggered for contraction
I band = actin (thin) only zone
A band = overlap zone of actin and myosin
M line = middle of the Z discs
Z disc = from one Z disc to another is the length of the sarcomere
H zone = made up of only myosin
What is the structure of the thin filament? What are the different components?
tropomyosin backbone
- has actin heads attached
- has troponin C - calcium binding site
- has troponin T = tropomyosin binding site
tropomyosin blocks the active site on actin for myosin head binding
- blocks contraction
What is the contractile cycle? What are the different stages?
primed myosin head, binding, power stroke, detachment and repeat
primed myosin head
- myosin head has different configurations
- low energy configuration is bound to ATP, not primed and unable to bind to actin active site
- ATP hydrolysis primes the myosin head = cocks the head upright in high energy configuration
binding
- primed myosin head with ADP and Pi attached form a cross bridge with actin
- formation of cross bridge causes release of Pi
- calcium released binds to troponin C and pulls it out of the way to expose the active site on actin
- myosin head binds with actin on the active site
power stroke
- ADPis released and myosin undergoes a conformational change
- pulls the actin filaments inward towards the centre of the sarcomere
detachment
- ATP binds to myosin making it go back to its original low energy configuration
- change in configuration causes myosin to release from actin
What are the different mechanisms that cause a rise in calcium concentration?
receptor mediated
- binding of a ligand to the receptor on the endoplasmic reticulum causes the calcium channels to open and influx
voltage gated calcium channels
- action potential causes opening of channels and influx
What are the properties of the skeletal muscle? t-tubules? filament arrangement? calcium sensor? calcium release? contraction mechanism?
multi-nucleated, voluntary muscle (CNS)
- t-tubules are present
- filament arranged in a striped pattern
- calcium sensor is troponin
- calcium release
= voltage gated channel via the dihydropyridine receptors
= ligand gated channels via the ryanodine receptors - contraction mechanism is the removal of suppressive troponin = loses NO mechanism
What are the properties of the cardiac muscle? t-tubules? filament arrangement? calcium sensor? calcium release? contraction mechanism?
mono-nucleated or bi-nucleated, involuntary muscle (ANS)
- t-tubules are present
- filament arranged in a striped pattern
- calcium sensor is troponin
- calcium release
= voltage gated channel via the dihydropyridine receptors
= ligand gated channels via the ryanodine receptors - contraction mechanism is the removal of suppressive troponin = loses NO mechanism
What are the properties of the smooth muscle? t-tubules? filament arrangement? calcium sensor? calcium release? contraction mechanism?
mono-nucleated , involuntary muscle (ANS)
- t-tubules are not present
- filament arranged in a mesh not striped pattern
= do not shorten at contraction instead they twist
= interact with the membrane at a dense circular body
- calcium sensor is calmodulin (no troponin)
- calcium release
= tyrosine kinase linked receptor
= G protein coupled receptors
= voltage gated calcium channels
- contraction mechanism is activation of the myosin light chain kinase (MLCK) = GO mechanism
What happens at the neuromuscular junction for skeletal muscles?
How does the nervous system communicate with the skeletal muscle and bring about muscle contraction?
What is excitation contraction coupling of the neuromuscular junction? (sequence of events)
action potential arrives at the pre synaptic membrane
- sodium channels open and there is an influx of sodium ions. if threshold value for membrane potential is reached then action potential occurs
AP stimulates calcium channels opening
- influx of calcium ions
calcium ions stimulate vesicles containing neurotransmitter to fuse with the pre-synaptic membrane and release NT into the synaptic cleft
NT binding to post synaptic membrane receptors opens ligand gated channels
- depolarises muscle
NT must release receptor to enable contraction
muscle motor end plate (NM junction) is depolarised and AP travels down the t-tubule
depolarisation causes conformation change in the physically associated dihydropyridine receptors
- DHPR binds dihydropyridines
DHP physically interacts with the sarcoplasmic reticulum
DHP conformation change causes ryanodine receptors on the SR to open
- influx of calcium ions
calcium interacts with troponin C
- priming of myosin, crossbridge, power stroke, detachment
What happens at the neuromuscular junction for cardiac muscles?
How does the nervous system communicate with the skeletal muscle and bring about muscle contraction?
What is excitation contraction coupling of the neuromuscular junction? (sequence of events)
action potential arrives at the pre synaptic membrane
- sodium channels open and there is an influx of sodium ions. if threshold value for membrane potential is reached then action potential occurs
AP stimulates calcium channels opening
- influx of calcium ions
calcium ions stimulate vesicles containing neurotransmitter to fuse with the pre-synaptic membrane and release NT into the synaptic cleft
NT binding to post synaptic membrane receptors opens ligand gated channels
- depolarises muscle
NT must release receptor to enable contraction
muscle motor end plate (NM junction) is depolarised and AP travels down the t-tubule
depolarisation causes conformation change in the physically associated dihydropyridine receptors
- DHPR binds dihydropyridines
DHP is not physically coupled with the sarcoplasmic reticulum
DHP conformation change causes calcium release from calcium channels
calcium induced calcium release = CICR
- calcium ions induce calcium release from the SR by stimulating the RyR to open
- influx of calcium ions
calcium interacts with troponin C
- priming of myosin, crossbridge, power stroke, detachment
What is the difference between skeletal muscle contractions?
single twitch?
summation?
tetanus?
single twitch
- regularly spaced electrical impulses
summation of twitches
- second AP is introduced too early and there is no refractory/relaxation period
- increased tension
tetanus = lock jaw
- painful muscle contractions
- continuous contractions, fused APs
What is the sarcoplasmic reticulum? What is its role?
acts as an intracellular store for calcium
- SR membrane has numerous pumps which use ATP to pump calcium into the SR
- calcium within the SR is released into the cytoplasm through the ryanodine receptors = interact with the myofilaments and bring about muscle contraction
What are the roles of the smooth muscle?
Homeostatic role
- control fluid = movement
- sphincters = opening and closing
Tonic contractions
- support tubes
- move products
Slow contractions = slow twitch muscle
- little fatigue = have high endurance
- low O2 use
What is the difference between duration of skeletal, cardiac and smooth muscle contraction?
skeletal - fastest
cardiac - middle = plateau
smooth - slowest
