The Neuromuscular Junction and Cross Bridge Cycling

Question 1

muscle fiber contraction

Answer 1

• decision to move is activated by the brain - a signal is transmitted down the spinal cord to motor neurons
• motor neurons activate muscle fibers
• neurons and muscle cells are excitable cells - capable of action potentials - capable of changing their resting membrane potentials

Question 2

resting membrane potential

Answer 2

voltage across the plasma membrane

Question 3

action potential

Answer 3

type of electrical signal - a large change in resting membrane potential
- action potentials are converted to chemical signals to cross the synaptic cleft (small gap between cells)
- action potential crosses from a neuron to a muscle cell via a neurotransmitter - acetylcholine (Ach)

Question 4

Ion channels

Answer 4

rapidly changing the membrane potential in neurons and muscle cells requires the opening/closing of channels
- allow some ions to pass and not others
- movements of ions through channels changes membrane voltage
- two classes of ion channels: chemically and voltage gated

Question 5

chemically gated ion channel

Answer 5

opened by chemical messengers such as neurotransmitters

Question 6

voltage-gated ion channels

Answer 6

open/close in response to voltage changes - underlie all action potentials

Question 7

small depolarizations

Answer 7

in skeletal muscle fibers, chemically gated ion channels cause small depolarizations. small depolarizations trigger voltage gated ion channels to create action potentials

Question 8

anatomy of a motor neuron

Answer 8

• skeletal muscles are stimulated by somatic motor neurons
• axons: long, threadlike extensions of motor neurons; travel from central nervous system to skeletal muscle
• each axon divides into many branches as it enters a muscle
• each axon branch terminates in an axon terminal
• axon terminals form neuromuscular junctions (motor end plates) w muscle fibers
• each muscle fiber has only one neuromuscular junction

Question 9

anatomy of a neuromuscular junction

Answer 9

axon terminal and muscle fiber are separated by a gel-filled space; synaptic cleft
- synaptic vessels: membrane-bound sacs stored within the axon terminal; contain Ach
- on muscular fiber side, infoldings of sarcolemma called junctional folds contain millions of ACh receptors
- neuromuscular junction = axon terminal + synaptic cleft + junctional folds

Question 10

four steps that allow skeletal muscle contraction

Answer 10

1. events at the neuromuscular junction
2. muscle fiber excitation
3. excitation-contraction coupling
4. cross bridge cycling

Question 11

first 3 steps of events at the neuromuscular junction

Answer 11

1. action potential arrives at the axon terminal
2. voltage-gated ca2+ channels open; ca2+ ions enter the motor neuron
3. entry of ca2+ ions causes the release of ACh neurotransmitter into the synaptic cleft via exocytosis

Question 12

steps 4 and 5 of events at the neuromuscular junction

Answer 12

4. ACh diffuses across the synaptic cleft to ACh receptors in the junctional folds
5. ACh binding opens chemically gated ion channels

Question 13

steps 6/7 of the events at the neuromuscular junction

Answer 13

6. na+ ions enter the muscle fiber and k+ ions exit the muscle fiber. net movement of na+ creates local change in membrane potential/end plate potential
7. once the membrane potential hits a threshold value (abt -55mv) an unstoppable action potential propagates along the sarcolemma
   - Ach is degraded by acetylcholinesterase and diffuses away from the junction. this stops neural transmission to the muscle fiber

Question 14

myasthenia gravis

Answer 14

autoimmune disease in which the immune system destroys ach receptors
- symptoms caused by shortage of ach receptors:
- dropping eyelids
- difficulty swallowing
- difficulty talking
- generalized muscle weakness

Question 15

aesthetic botox

Answer 15

botulinum toxin
- reduces the amount of ach released from the motor neuron - decreases muscle contraction (reducing wrinkles)

Question 16

muscle fiber excitation

Answer 16

• resting sarcolemma is polarized - a voltage exists across the membrane, cell’s interior is negative compared to the outside
• action potentials result from predictable sequences of electrical changes
  occurs in 3 steps
• generation of end plate potential (epp)
• depolarization
• repolarization

Question 17

muscle fiber excitation: depolarization

Answer 17

generating and propagating an AP
- if epp causes enough of a change in membrane voltage to reach a critical level called threshold, voltage-gated na+ channels in the membrane will open
- large influx of na+ triggers an AP
- AP is unstoppable - leads to muscle fiber contraction
- AP spreads across sarcolemma from one voltage-gated na+ channel to the next causing additional depolarizations

Question 18

muscle fiber excitation: repolarization

Answer 18

restoration of normal electrical resting conditions
- na+ voltage-gated channels close; k+ voltage-gated channels open
- k+ effluxes out of the cell; restores initial resting membrane potential

Question 19

refractory period

Answer 19

muscle fiber cannot be stiumlated for a specific amount of time - until repolarization is complete
- ionic resting state is restored by na+-k+ pumps
- na+ is pumped back out, k+ is pumped back in

Question 20

excitation contraction coupling

Answer 20

events that transmit an ap along the sarcolemma (muscle fiber excitation) are couples to the sliding of myofilaments (contraction)
- aps are brief and end before any contraction is seen
- an ap doesn’t act directly on the myofilaments - it triggers a rise in intracellular ca2+
- an ap is propagated along sarcolemma and down into t tubules
- voltage sensitive proteins in t tubules stimulate the release of ca2+ from SR
- release of ca2+ leads to muscle fiber contraction

Question 21

cross bridge cycling relaxed

Answer 21

• at low intracellular ca2+ concentration
  
  • 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 t tubules change shape and cause SR to release ca2+

Question 22

cross bridge cycling contracting

Answer 22

• at higher intracellular ca2+ concentration
  
  • ca2+ binds to troponin
  • troponin changes shape and moves to tropomyosin away from myosin-binding sites
  • myosin heads bind to actin and form cross bridges
• cycling is initiated leading to sarcomere shortening and muscle fiber contraction
• when nervous system stimulation ceases, ca2+ is pumped back into the SR and contraction ends

Question 23

4 steps of cross bridge cycle

Answer 23

1. cross bridge formation
2. working (power) stroke
3. cross bridge detachment
4. cocking of myosin head
   * cross bridge cycles will repeat as long as actin’s binding sites are uncovered. cycles will cease when ca2+ moves back into SR, troponin changes shape, and tropomyosin covers actin’s binding sites

Question 24

cross bridge formation

Answer 24

high energy myosin head attaches to the thin filament’s active site

Question 25

working ( power ) stroke

Answer 25

myosin head pivots and pulls the thin filament towards the m line

Question 26

cross bridge detachment

Answer 26

atp attaches to myosin head, cross bridge detaches

Question 27

cocking of myosin head

Answer 27

energy from hydrolysis of atp cocks myosin head back into high energy state

Question 28

rigor mortis

Answer 28

• 3-4 hours after death, skeletal muscles begin to stiffen (peak @ 12hrs)
• atp isn’t being synthesized so intracellular ca2+ levels increase - ca2+ can no longer be pumped back into SR
• higher levels of ca2+ promotes cross bridge formation
• without atp myosin heads stay bound to actin site, constant state of contraction
• muscles will stay contracted until muscle proteins break down and myosin is released