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Human Physiology > Neuromuscular junction + muscles > Flashcards

Neuromuscular junction + muscles Flashcards

1
Q

What is the neuromuscular junction?

A

Found between a neuron and muscle cell. Site of communication between the two.

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2
Q

What are the steps of transmission through the neuromuscular junction?

A
  1. AP travels down motor neuron to presynaptic terminal
  2. Activation and opening of the voltage-gated Ca2+ channels (triggered by AP)
  3. ACh-containing vesicles fuse with the post-synaptic membrane and release ACh (neurotransmitters)
  4. Binding of neurotransmitter to ligand-gated ion channels on muscle (post-synaptic cell), cause change in membrane permeability, and opening of ion channels (may or may not cause AP).
  5. ACh broken down by acetylcholinesterase (AChE) - preserve + recycle / recirculate
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3
Q

Describe the nicotinic acetylcholine receptors

A
  • Transmembrane protein complex composed of 5 subunits
  • Acetylcholine binds to the 2 alpha subunit - 1 molecule per subunit (binds directly to channel to open - change conformation)
  • Located at NMJ and at postganglionic cells of vertebrate autonomic
  • Acts via fast transmission
  • binds nicotine and acetylcholine
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4
Q

Describe the muscarinic receptors

A
  • G-protein coupled receptors
  • Acetylcholine binds to G-protein coupled receptor (not directly to channel)
  • Activation of G-protein complex on cytoplasmic side (cascade of biochemical reactions that open channel)
  • Alpha-subunit activation - can act directly on the ion channels or effector protein and intracellular messengers
  • Acts via slow transmission
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5
Q

Describe the steps of the use of a voltage clamp of skeletal muscle cell

A
  1. Voltage clamp muscle using 2 electrodes, and simultaneously electrically stimulate the presynaptic motor neuron
  2. Stimulation of motor neuron will cause the release of acetylcholine from the presynaptic motor neuron
  3. This will enable you to record macroscopic end plate currents (EPCs)
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6
Q

Describe the end plate potential

A

nAchR opening creates an excitatory postsynaptic potential in the muscle, triggering the opening of voltage-gated Na+ and K+ channels along a muscle fiber.
Leads to a suprathreshold (greater than threshold) and therefore an action potential in the skeletal muscle - causes muscle contraction
- Muscle has membrane potential lower than -70 mV (diff permeabilities to ions + diff concentrations) -70 to -60 for threshold (goes up +30mV-40mV approximately).

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7
Q

Are EPPs and APs the same?

A

They are not, EPPs trigger APs. ACh-induced depolarization causes End Plate Potential (EPP) - happen @ neuromuscular junction

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8
Q

Describe Myasthenia gravis (pathophysiology of NJM)

A

A chronic neuromuscular disease that is characterized by weakness in skeletal muscles. Occurs due to autoantibodies that attack the nicotinic acetylcholine receptor (block receptor - partial or fully, very little muscle stimulation). ACh in the synaptic cleft cannot bind to receptors - broken down by acetylcholinesterase (AChE inhibitor) - allows ACh to be in the synaptic cleft for longer. Reduced EPP and muscle contraction.

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9
Q

What is Cogan’s eyelid twitch?

A

Tool to diagnose Myasthenia gravis.
- Eyelid twitch response (Cogan’s eyelid twitch) - first symptom of MG - up and down when they look left and right
-Elicited by looking down and then straight
- 57yo woman - normal brain MRI, generalized weakness
- MG was confirmed by repetitive nerve stimulation and positive anti-nAChR binding antibody test
- Take a lot of current to stimulate action potential

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10
Q

Describe the components from large to small of a tendon

A

Tendon - muscle - artery, vein, nerve - muscle fascicle (cell bundle) - muscle fiber (muscle cell) - myofibril - Sarcomere - Actin + myosin (thick and thin filaments)

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11
Q

What is the triad?

A

When sarcoplasmic reticulum meets the t-tubule. Has ions around, these ends are called terminal cisterna (little well)

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12
Q

Describe the architecture of skeletal muscle

A

Have lots of mitochondria to produce lots of ATP.

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13
Q

What is the sarcoplasm?

A

Cytoplasm of the muscle cell

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14
Q

What is sarcolemma

A

Plasma membrane of the muscle cell

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15
Q

Describe the myofibril

A

Organelle composed of bundles of myofilaments. A muscle cell (or muscle fiber) is composed of a bundle of myofibrils. Surrounded by sarcollema + multiple nuclei. Striated appearance - darker and lighter bands. *Composed of repeating units of contractile proteins = sarcomeres = contractile unit of myofibril (has two z lines on either side). Approximately 100,000 sarcomeres in bicep brachii from one end to the other.

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16
Q

What is the thick filament?

A

Made of intertwined proteins called myosin - appears darker

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17
Q

What is the thin filament?

A

Made of intertwined strands of protein called actin - appears lighter

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18
Q

What is the m line?

A

Center of sarcomere; provides anchoring for myosin and elasticity.

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19
Q

What is the I-band?

A

Zone not covered by myosin. Lighter area, no overlap, on either side of sarcomere, only actin.

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20
Q

What is A-band?

A

Covers the length of the myosin band (+some actin). The area of structural overlap in the middle of sarcomere - both actin and myosin.

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21
Q

What is the z-disc?

A

Defines the boundary of one sarcomere. Made of large proteins for anchoring.

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22
Q

Define Actin

A

Globular protein linked to form helical strands. Each has one myosin binding site. Associated with two regulatory proteins (Tropomyosin, troponin).

23
Q

Define Tropomyosin

A

Rod-shaped protein composed of two alpha helical chains wrapped in a supercoil. Found in grooves made by actin. Partially covers the myosin binding site.

24
Q

Define Troponin

A

Three protein complex attached to both actin and tropomyosin. Holds tropomyosin over myosin binding site on actin.
-Troponin A - binds to actin
-Troponin C - binds calcium
-Troponin T - binds tropomyosin

25
Q

What makes up the thin filament?

A

Actin, tropomyosin, and troponin complex.

26
Q

What makes up the thick filaments?

A

Myosin

27
Q

Define Myosin

A

Protein made of two long polypeptide strands, each forming part of the tail, hinge, arm and head. Head has actin binding site and an ATP binding site (location of ATPase) - when hydrolyzed, changes conformation of head. Undergoes conformational change to generate contraction.

28
Q

What happens to the sarcomere during a muscle contraction?

A

Crossbridge formation - Actin binds Myosin, it’s like Actin is crowd surfing Myosin. Size of Actin and Myosin does not change, but sarcomere gets smaller. M zone gets smaller - actin filaments get closer - sarcomere gets smaller. More overlap of Actin and Myosin. Lose I bands in contraction.

29
Q

Describe the sliding filament theory

A

During contraction:
- binding of myosin to actin forms a crossbridge
- myosin head changes shape and a power stroke occurs
- actin slides past myosin - sarcomere shortens

30
Q

Describe the steps from the NMJ signalling to muscle contraction

A
  1. AP travels down the motor neuron, causing ACh release from pre-synaptic motor neuron
  2. AP travels down the T-tubule, to dihydropyridine (DHP) receptor - DHP senses voltage change - leading to change in conformation
  3. DHP receptor opens (pulls on ryanodine when DHP undergoes conformational change) ryanodine receptor (Ca2+ release channel) on terminal cisterna of SR (SR is rich in calcium - rushes out when opened)
  4. Ca2+ is released from lateral sac of SR (terminal cisterna)
  5. Ca2+ binds to receptors in the sarcomere, to inititate a muscle contraction - binds troponin C (usually blocks the myosin binding site on actin, Ca2+ pushes it away from binding site)
  6. Myosin binds to actin, in a crossbridge formation
  7. Contraction
  8. Free Ca2+ is recycled back into the SR through Ca2+ ATPase
  9. Ca2+ dissociates from Troponin C, going down its concentration gradient (into the cytoplasm, then uses active transport - ATPase into the SR)
  10. Tropomyosin then covers the myosin binding site on actin, being stabilized by Troponin - myofilaments in relaxed position
    *All steps actually happen @ same time
31
Q

Describe the Actin-myosin ATP cycle

A
  1. New ATP attaches to myosin head - crossbridge detaches (low affinity in this state)
  2. New ATP is converted to ADP and Pi - myosin head energized and ready to bind (high affinity state for actin)
  3. Myosin has high affinity for actin - crossbridge formation
  4. Pi is released - power stroke - actin slides over myosin, pulling on the Z line, ADP is released.
    *ATP is the limiting factor in this cycle- without, there is no crossbridge formation
32
Q

Function an supply of ATP?

A
  1. Calcium ATPase
  2. Activation of Myosin head
  3. Neurotransmitter vesicles
  4. Re-storing membrane potential
    *don’t really understand?
33
Q

What is a motor unit?

A

One motor neuron + muscle fibers it inervates. When motor neuron is activated - innervates all muscle fibers.

34
Q

What is a muscle twitch?

A

Muscle contraction caused by a single AP in the motor neuron.
Duration of twitch: 10-100 ms, depends on fiber type

35
Q

What is latency?

A

Time between an AP and the initiation of contraction. (Takes time for AP to travel down T-tubule).

36
Q

Describe grading muscle contraction

A

Increased force of contraction

37
Q

What is motor unit recruitment?

A

As more motor units are recruited, more muscle fibers contract - higher contractile force
*Muscle fibers of different motor units are intermingled, so the forces applied to the tendon remain roughly balanced regardless of which motor units are stimulated - larger muscle = more units

38
Q

Describe summation of twitch contractions

A

Increased stimulus frequency - can add twitches (not APs) because there is no absolute refractory period for twitches

39
Q

Describe varying stimulus frequency

A

As stimulus (AP) frequency is increased, the muscle twitch has less time to relax before next contraction (doesn’t complete relaxation time)

40
Q

What is tetanic contraction?

A

Stimulus is so frequent that there is no relaxation. Say the muscle is in tetanus.
There exists unfused and fused tetanus (muscle can’t contract anymore).

41
Q

What are the key differences between skeletal and smooth muscle?

A
  • location
  • shape
  • involuntary movement
  • nucleus
  • striation
42
Q

State the main features of skeletal muscle

A
  • Fibers: striated, tubular and multi nucleated
  • Voluntary
  • Usually attached to skeleton
43
Q

State the main features of smooth muscle

A
  • Fibers: non-striated, spindle-shaped, and uninucleated
  • Involuntary
  • Usually covering wall of internal organs (found in organs, GI tract, blood vessels) - helps with digestion + blood flow
  • 1 nucleus
  • no motor unit, 1 neuron with finger like projections
44
Q

What is the structure of smooth muscle?

A

Has 2 layers - oriented at right angles to each other
- longitudinal layer, contributes to dilation and shortening
- Circular layer, organ constriction and elongation

45
Q

What is the neuroeffector junction?

A

Autonomic neurons.
Junction between preganglionic neurons (cell body in CNS) and ganglion. Postganglionic neurons (cell body in ganglion, terminates on target tissue/organ - smooth muscle).
No motor end plate.
Varicosities - main neurotransmitters: norepinephrine, acetylcholine. Must be close to target.
Diff from skeletal muscle, inhibitory + excitatory.
Wide surface area (advantage of this diffusion).

46
Q

What is found in smooth muscle that is similar to the Z line in skeletal muscle?

A

Dense body.

47
Q

How are actin and myosin arranged in smooth muscle?

A

Actin + myosin are arranged in diagonal filaments, and converge @ dense body.

48
Q

Compared to skeletal muscle, what is different in smooth muscle?
*neuromuscular junction vs neuroeffector junction

A
  • missing motor end plate
  • pre-synaptic neuron to muscle distance: bigger distance in smooth muscle
  • binding flexibility of NT: more flexible in smooth muscle
  • Types of NT: Norepinephrine and acetylcholine in smooth muscle
    -One nucleus in smooth muscle, many in skeletal
  • Actin + myosin not located in sarcomeres - diagonal arrangment, no regular overlap pattern
  • structure + organization of the fibers
  • filaments attached to dense bodies
  • dense body acts like Z line - filaments pull on dense body and the muscle contracts
  • presence of calveolae in smooth muscle - indentations on the sarcolemma (calcium stores)
49
Q

Describe the steps of signalling in neuroeffector junction

A
  1. Action potential arrives at the varicosity
  2. Depolarization opens voltage-gated Ca2+ channels.
  3. Ca2+ entry triggers exocytosis of synaptic vesicles
  4. NE binds to adrenergic receptor on target (G-coupled receptor)
  5. Activity ceases when NE diffuses away from the synapse
  6. NE is transported back into the axon
  7. NE can be taken back into synaptic vesicles for re-release
  8. NE is metabolized by monoamine oxidase (MAO)
    *recycling of neurotransmitters does not occur with skeletal muscle
50
Q

Which receptors do acetylcholine and norepinephrine bind respectively?

A

Acetylcholine - muscarinic cholinergic receptor
Norepinephrine - adrenergic receptor

51
Q

Similarities between smooth + skeletal muscle

A
  • Contraction relies on actin and myosin interaction
  • responds to increase in calcium within the cell
  • ATP used for cross-bridge formation
52
Q

Describe the steps of the excitation contraction coupling in smooth muscle

A
  1. Ca2+ most comes from ECF through a CaVTG (or VGCC) - only small amount from SR
  2. Ca2+ binds to calmodulin (protein activated by Ca)
  3. Myosin inactive
    4.Calmodulin activates kinases - transfer of Pi to myosin head - active state - myosin phosphorylated
  4. Crossbridge formation and power stroke
  5. Phosphorylases remove phosphate from myosin heads when Ca2+ levels fall
53
Q

What does Calmodulin do?

A
  1. Binds Ca2+
  2. Activates myosin light chain kinase - leads to myosin head activation
  3. Filament structure - Thin filament, is made of actin, tropomyosin, caldesmon and calmodulin (14:2:1:1)
  4. Calmodulin regulates activity of caldesmon (variety of roles including regulating tropomyosin).

Human Physiology (13 decks)

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