Neuromuscular Junction and Cross Bridge Cycling Study Guide Flashcards

1
Q

what activates muscle fibers

A

Motor Neurons

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1
Q

Define resting membrane potential

A

voltage across the plasma membrane

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2
Q

Average resting membrane potential of a muscle cell is: _______.

A

~70mV

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3
Q

Define action potential.

A

A type of electrical signal - a large change in resting membrane potential

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4
Q

Action potentials are converted to ______ to cross the ________.

A
  • chemical signals
  • synaptic cleft
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5
Q

Define synaptic cleft.

A

The small gap between cells

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6
Q

Define neurotransmitters

A

chemical messengers, an action potential crosses from a neuron to a muscle cell via a neurotransmitter

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7
Q

What neurotransmitter crosses from a motor neuron to a muscle cell?

A

Acetylcholine (Ach) crosses from a motor neuron to a muscle cell

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8
Q

Where specifically does this neurotransmitter bind on the muscle cell?

A

ach receptors embedded in the sarcolemma in the neuromuscular junction on the muscle cell

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9
Q

Compare and contrast chemically-gated and voltage-gated ion channels

A
  • Chemically-gated ion channels: opened by chemical messengers such as neurotransmitters
    Example: Ach receptors on muscle cells
  • Voltage-gated ion channels:
    open/close in response to voltage changes - underlie all action potentials
    Example: t-tubules
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10
Q

How do chemically-gated and voltage-gated ion channels work together in skeletal muscle fibers?

A

Chemically gated ion channels cause small depolarizations. Small depolarizations trigger voltage-gated ion channels to create small action potentials

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11
Q

Define axon

A

Axon: long, threadlike extensions of motor neurons; travel from central nervous system to skeletal muscle (bundle of axons = nerves)

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12
Q

What are the smallest branches of an axon called

A

axon terminal

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13
Q

What are the 3 components of the neuromuscular junction?

A

Axon terminal
Synaptic cleft
Junctional folds

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14
Q

Define synaptic vesicles. What does it contain?

A
  • membrane-bound sacs stored within the axon terminal
  • Contains millions of ACh receptors
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15
Q

myasthenia gravis

A

immune system destroys ACh receptors, which are needed to open the chemically gated channels to allow movement of Na+ and K+ to change the membrane potential and eventually cause an action potential. This is caused by toxins, drugs, and diseases that interfere with events at the neuromuscular junction. Causes symptoms such as drooping eyelids, difficulty swallowing, difficulty talking, generalized muscular weakness

16
Q

Botox(botulinum toxin)

A

less ACh is diffused in the neuromuscular junction, which means there will be fewer action potentials, and therefore fewer muscle contractions. The decreased muscle contractions lead to less wrinkles.

17
Q

What ion influxes into a muscle cell in depolarization

A

Na+ influxes into a muscle cell in depolarization

18
Q

What ion effluxes out of a muscle cell in repolarization

A

K+ effluxes out of the cell

19
Q

After depolarization, how does an AP travel along the sarcolemma surface?

A

AP spreads across sarcolemma from one voltage-gated NA+ channel to the next causing additional depolarizations

20
Q

Define refractory period.

A

Muscle fiber cannot be stimulated for a specific amount of time - until repolarization is complete.

21
Q

How do Na+-K+ Pumps restore ionic resting state?

A

Restored by Na+-K+ pumps – Na+ is pumped back out, K+ is pumped back in

22
Q

Be ready to define the parts of an action potential from a graphical representation

A

Beginning of upwards slope: Na+ channels open
Top of upwards slope: depolarization due to NA+ entry
Top of downwards slope: NA+ channels close, K+ channels open
Middle of downwards slope: repolarization due to K+ exit
Flat line after slope: K+ channels closed

23
Q

An action potential traveling along the sarcolemma dives down into the ______. This action potential triggers the release of ____ from the ___________.

A
  • t tubules
  • ca2+
    sarcoplasmic reticulum (SR)
24
Q

In terms of cross bridge formation, what happens when intracellular levels of Calcium are low?

A

Tropomyosin blocks the active sites on actin
Myosin heads cannot attach to actin
Muscle fiber remains relaxed
In response to AP, voltage-sensitive proteins in the t-tubules change shape and cause sarcoplasmic reticulum to release Ca2+

25
Q

In terms of cross bridge formation, what happens when intracellular levels of Calcium are high?

A

Ca2+ binds to troponin
Troponin changes shape and moves tropomyosin away from myosin-binding sites
Myosin heads can bind to actin and form cross bridges
Cycling is initiated leading to sarcomere shortening and muscle fiber contraction

26
Q

What happens to calcium when nervous stimulation ceases?

A

Ca2+ is pumped back into the SR and contraction ends

27
Q

4 steps of cross bridge formation

A
  1. Cross bridge formation: high-energy myosin head attaches to the thin filament’s active site
  2. Working (power) stroke: myosin head pivots and pulls the thin filament towards the M line
  3. Cross bridge detachment: ATP attaches to myosin head, cross bridge detaches
  4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head back into high-energy state
28
Q

In what step of cross bridge formation does ATP bind? In what step is ATP hydrolyzed?

A

ATP is hydrolyzed in the 4th step
ATP binds in the 3rd step

29
Q

What clinical impact(s) does the necessity of ATP have? Think about what happens when we’re no longer making ATP!

A

Without ATP, the cross bridges cannot detach, causing muscles to be stiff and in a constant state of contraction. (rigor mortis)