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MSK Summative > Muscle Contraction > Flashcards

Muscle Contraction Flashcards

1
Q
  • What are T-Tubules in myofibrils extensions of?
  • What is their function?
A
  • extensions of plasma membrane (sarcolema)
    • a tubular invagination of the sarcolemma of skeletal muscle fibers that surrounds myofibrils as the intermediate element of the triad in skeletal muscle
  • Function:
    • involved in transmitting the action potential from the sarcolemma to the interior of the myofibril.
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2
Q

In skeletal muscle, what makes up the triad?

A

1 t-tubule and 2 terminal cisternae

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3
Q
  • What are the 7 steps of muscle contraction in a myofibril?
    • Which bands are shortened?
    • Which bands stay the same length?
A
  1. Depolarization of motor end plate (via Na+ channels) travels along muscle cell and down T-tubule
  2. Depolarization of the voltage sensitive dihydropyridine receptor, mechanically coupled to the ryanodine receptor on the SR
    • induces a conformational change in both receptors, causing Ca2+ release from sarcoplasmic reticulum.
  3. Release Ca2+ binds to troponin C, causing a conformational change that moves tropomyosin out of myosin binding groove on actin filaments
  4. Myosin releases ADP and Pi—-> displacement of myosin on the actin filament (power stroke)
    • contraction results in shortening of the H and I bands between the Z lines
    • A band remains the same length
  5. Binding of new ATP molecule causes detachment of myosin head from actin filament
    • hydrolysis of bound ATP—> ADP causes myosin head to adopt high energy position (“cocked”) for the next contraction cycle
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4
Q

What are two main differences between skeletal and smooth muscle?

A
  • Skeletal:
    • nucleus located peripherally
    • multiple nuclei per cell
  • Smooth muscle
    • nucleus located centrally
    • one nuclei per cell
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5
Q
  • What is a sarcomere?
    • What is it a component of?
A
  • Myofilament
    • area between 2 Z lines
    • composed of thin (actin) and thick (myosin) filaments
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6
Q

Components of Myofilament:

  • A band
  • I band
  • H band
  • M line
  • Z line

What are they made of? How do they change (or not) shape?

A
  • A band:
    • “dark” part of skeletal muscle straitions
    • remain constant in width
    • composed of all of myosin (thick) and some actin (thin)
  • I band:
    • “light” part of skeletal muscle straition
    • Composed only of thin filaments (actin)
    • Changes in size (smaller with contraction)
  • H band:
    • bisects A band (1/2)
    • composed only of thick filament (myosin)
    • changes in size (smaller with contraction)
  • M line:
    • bisects the H band
    • attachment site of thick filament (myosin)
  • Z line:
    • dark lines that bisect I bands
    • attachment site of thin filaments
    • separates each sarcomere
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7
Q
  • Function of terminal cisternae?
    • What are they a part of?
A
  • Terminal cisternae are enlarged areas of the sarcoplasmic reticulum surrounding the transverse tubules.
    • make up triad (with t-tubule)
  • Function:
    • store calcium
      • (increasing the capacity of the sarcoplasmic reticulum to release calcium)
    • release it when an action potential courses down the transverse tubules, eliciting muscle contraction.
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8
Q

Definitions of:

  • Sarcolemma
  • Sarcoplasm
  • Sarcoplasmic Reticulum
  • Myofibrils
  • Myofilaments
  • Sarcomeres
A
  • Sarcolemma
    • plasma membrane of skeletal muscle cell
  • Sarcoplasm
    • cytoplasm
  • Sarcoplasmic Reticulum
    • endoplasmic reticulum
  • Myofibrils
    • cylindrical organelles found inside skeletal muscle cells
  • Myofilaments
    • filaments of a myofibril
    • organized into repeating units called sarcomeres
  • Sarcomeres
    • regions between two successive Z lines
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9
Q

What is the rate limiting step of Synaptic Transmission at the neuromuscular junction?

A
  • Ca2+ diffusion into and through the axon terminal to the snare proteins
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10
Q

What are the 3 main SNARE proteins and what are they attached to?

A
  • Synaptobrevin (v-SNARE)
    • attached to vesicles
  • Syntaxin and SNAP 25 (t-SNARE)
    • attached to presynaptic membrane
  • Synaptotagmin
    • Ca2+ sensor that triggers the actual fusion event
      • makes other SNARE proteins twist together to pull vesicle down for fusion and exocytosis
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11
Q
  • What 2 things make up choline acyltransferase (ACh)?
    • Enzyme?
    • Where is it made?
A
  • ACh= Choline + Acetyl CoA (from Kreb’s cycle)
    • via choline acetyltransferase
  • Made in:
    • cystoli neuron soma (body) and transferred to axon terminal
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12
Q

ACh remains in synaptic space for very short time (ms)

  • What is ACh broken down into?
    • enzyme?
    • where does this happen?
A
  • broken down into:
    • acetate: diffuse out
    • choline: always recycled
  • via acetylcholinesterase
  • in synaptic cleft
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13
Q
  • How does ACh get from the Soma to the NMJ?
    • proteins
    • types of transport?
A
  • Kinesin (to axon from cell body)
    • fast or slow anterograde
  • Dynein (from soma to axon)
    • fast retrograde
  • Microtubules
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14
Q
  • What types of channels are ACh (nicotinic)?
    • What mostly enters?
A
  • nonselective cation channels: Na+, Ca2+, K+
    • Na+ wants to move inside due to [] gradient and electrical gradient
    • K+ wants to move outside but is attracted to the (-) charge inside cell so it gets stuck
    • Ca2+ doesn’t move in as much because it is larger (2+ charges)
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15
Q
  • How many subunits does the ACh receptor (nicotinic) have?
    • how many ACh need to bind to open the channel?
A
  • 5 subunits
  • need 2 ACh to open
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16
Q

What is the function of Ca in the presynaptic membrane of NMJ?

A
  • AP in nerve terminal open Ca2+ channel
    • Ca 2+ entry causes SNARE proteins to interact and fusion of vesicles for exocytosis
17
Q
  • What is the pathological mechanism of Myasthenia Gravis?
  • What is the clinical presentation?
    • symptoms?
  • What is it associated with?
A
  • Pathology: Autoimmune
    • B lymphocytes produce antibodies that bind AChRs, blocking ACh binding sides
  • Clinical presentation:
    • muscular weakness that gets worse during activity
  • Symptoms:
    • double vision
    • drooping eyelids
    • slurred speech
    • dysphagia
  • Associated with:
    • thymic hyperplasia or thymoma
18
Q

What are the three main mechanisms in which antibody binding causes Myasthenia Gravis?

A
  1. Less extensive junction folds (less SA), widened synaptic cleft (takes longer time and more chance of diffusion) and less AChR’s
  2. Antibody binding causes crosslinking of individual receptor by tagging them for degradation
    • receptor turnover rate increase by 3
  3. B lymphocytes produce antibodies that bind AChR’s, blocking ACh binding sites
19
Q
  • What is the pathology of Lambert Eaton Myasthenic Syndrome?
  • How does it present?
  • Paraneoplastic syndrome?
A
  • Pathology:
    • antibodies against presynaptic (P/Q type) Ca2+ channels at NMJ
  • Clinical presentation:
    • musuclar weakness (proximal arms and legs) that improves with activity
      • eyes are usually spared (different than MG)
  • Paraneoplastic syndrome:
    • small cell cancer of the lung
20
Q

Myasthenia Gravis vs. Lambert Easton Myasthenic Syndrome?

  • effect of cholinesterase activity
  • neurotransmission with repetitive stimulation
  • mainly affects where on body?
  • effect of activity on muscular weakness?
  • associated with which cancers?
A
  • Myasthenia Gravis: (post synaptic)
    • AChR agonists and acetylcholinesterase inhibitors helpful
    • reduced neurotransmission with repetitive stimulation
    • characteristic eye droop
    • muscular weakness gets worse with increased activity
    • associated with Thymic hyperplasia or Thymoma
  • Lambert-Eaton Myasthenic Syndrome: (presynaptic)
    • Anti-cholinesterase therapy is less effective
      • not enough ACh to begin with
    • Enhanced neurotransmission with repetitive stimulation
    • strongest affect seen in proximal limbs
      • no eye effects
    • muscular weakness improves with activity and exercise
    • associated with small cell carcinoma of lung
21
Q

In cross bridge cycle in muscle contraction:

  • what moves the myosin head?
  • what releases myosin from actin?
A
  • ATP binding releases myosin from actin
  • ATP hydrolysis move myosin head
22
Q
  • How are actin filaments attached to Z lines?
  • What attaches Z and M line proteins?
A
  • Actin filaments attach to Z line by alpha-actinin
  • Titin attaches Z and M line proteins
    • “springy”, recoils to restore length of sarcomere at relaxation
23
Q

What is the function of Desmin, Ankyrin and Dystrophin in myofilament?

A
  • Desmin and Ankyrin:
    • connect Z line to membrane
  • Dystrophin
    • connect actin to membrane at dystroglycan-sarcoglycan complex
24
Q

What does smooth muscle have instead of troponins?

A
  • Calmodulin
    • binding of 4 Ca2+ ions cause change in conformation and allows actin and myosin to bind
25
Q

What are the 2 sources of Ca2+ in smooth muscles?

A
  • Unlike skeletal muscle, smooth muscle is dependent on two sources of calcium in order to initiate contraction.
    • These two sources are:
    1. calcium sequestered in the S.R. of the smooth muscle cell.
    2. extracellular calcium that can enter the smooth muscle cell via calcium channels on the membrane of the smooth muscle cell.
26
Q
  • Role of myosin light chain kinase activity in smooth muscle contraction?
  • Role in relaxation?
A
  • Contraction:
    • Myosin light chain kinase (MLCK) is an enzyme that phosphorylates one of the two myosin light chains associated with the myosin head.
      • The MLCK hydrolyzes ATP and takes the inorganic phosphate (Pi) from the ATP and puts it on the myosin light chain.
      • Once the myosin light chain is phosphorylated, the myosin head develops a high affinity for the actin active site and binds readily to it.
  • Relaxation:
    • the myosin light chain that was phosphorylated by the MLCK must be dephosphorylated by the myosin light chain phosphatase mentioned previously.
    • Once the myosin light chain is dephosphorylated, the myosin head no longer has significant affinity for the actin active site and relaxation ensues.

MSK Summative (8 decks)

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