Structural Organization of skeletal muscle Flashcards

1
Q

Striated muscles are….

A

Cardiac and skeletal

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2
Q

Non-striated muscle is…

A

Smooth muscle

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3
Q

Voluntary muscle is?

A

Skeletal muscle

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4
Q

Involuntary muscle is?

A

Smooth and cardiac

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5
Q

What is the primary role of skeletal muscle?

A

To produce the force and movement necessary for life

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6
Q

What % of the body is skeletal muscle?

A

35-55%

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7
Q

Why is skeletal muscle voluntary?

A

Because its contraction is controlled by input from the nervous system via alpha motor neurons. It is an elastic and excitable cell.

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8
Q

How many muscles fibres synapse per motor neuron?

A

Alpha motor neurons branch and synapse onto a number of skeletal muscle fibres.

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9
Q

What is a ‘motor unit’?

A

A single alpha motor neuron and the muscle fibres it innervates

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10
Q

How is contraction modulated by recruitment?

A

The more motor units, and therefore muscle fibres that are recruited, the large the force and strength of contraction of the muscle.

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11
Q

What follows its electrochemical gradient INTO the excitable cell?

A

Ca2+ (1.5mM) —–> Ca2+ (0.1mM)

Na+ (145mM) ——-> Na+ (10mM)

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12
Q

What would follow its electrochemical gradient OUT of the cell?

A

K+ (145mM) ——–> K+ (4mM)

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13
Q

What is the size principle of recruitment?

A

“under load, motor units are recruited smaller –> larger. So smaller oxidative units that are more sensitive to change are recruited first, THEN large glycotic units.

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14
Q

What is the purpose of schwann cells?

A

To enable fast propagation of AP

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15
Q

What are the presynaptic events?

A

1) AP in the presynaptic cell reaches the nerve terminal
2) Depolarisation opens voltage gated Ca2+ channels, calcium follows its electrochemical gradient into the presynaptic cell
3) Ca2+ influx triggers exocytosis of vesicles containing neurotransmitter acetyl choline.
4) ACh diffuses across the synaptic cleft
5) ACh is broken down by acetylcholinesterase in the synaptic cleft

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16
Q

What happens to the pre-synaptic membrane?

A

It is recycled, so there is no net loss!

17
Q

What is within the presynaptic terminal boutons?

A

Mitochondria, neurotransmitters within vesicles, dense bar/active zone.

18
Q

What is the dense bar for?

A

Site of neurotransmitter release

19
Q

What are the steps of vesicle cycling?

A

1) Neurotransmitters are actively transported into synaptic vesicles
2) Synaptic vesicles gather at the active zone
3) synaptic vesicles dock at the active zone
4) vesicles are primed
5) converted into a state of competence for Ca2+ triggered pore opening
6-8) vesicles endocytose and recycle

20
Q

What generates End Plate Current (EPC)

A

The near synchronous bindings of more then 200,000 ACH receptor ion channels. 17,000 Na+ and less K+ leave, resulting in depolarisation

21
Q

What causes ACh to debind from ACh receptor ion channels?

A

Aceytlcholinesterase activity

22
Q

How is the falling time course of EPC determined

A

By the random closure of individual channels over a period of time

23
Q

Are AChR specific or non-specific?

A

Non-specific

24
Q

How big is the synaptic cleft ACh has to travel?

A

15nm

25
Q

How does acetylcholinesterase work

A

Hydrolyses ACH into choline and acetate

26
Q

Where does choline and acetate go post-hydrolysis?

A

Choline: diffuses back into the presynaptic terminal and is reabsorbed (to make more ACh)
Acetate: Diffuses into surrounding medium

27
Q

List the post synaptic events at the NMJ

A

1) 2 ACh molecules bind to ACh receptor ion channels
2) Channels open
3) Na+ inflow, K+ outflow
4) depolaristion of motor end plate occurs (EPP)
5) opening of Na+ voltage gated channels
6) Na+ inflow
7) depolarisation of muscle fibre
8) propagation of AP

28
Q

What comes first, EPP or EPC?

A

EPC. The movement of Na+ and K+ through ACh receptors causes the EPC, which in turn causes EPP

29
Q

Where would you find AChE and what does it do?

A

This enzyme is found anchored to the collagen fibrils of the basement membrane, where is hydrolyses ACh

30
Q

What can target AChE and what would happen if this occurred?

A

Insecticides and military nerve gases (sarin)

If this occurred ACh would not breakdown, would remain bound to AChR and the muscle would remain activated, in a state of rigor.

31
Q

What do presynaptic abnormalities affect?

A

Vesicle cycling and calcium channel opening

32
Q

What do Botulinum and tetanus do?

A

Prevent vesicle docking, muscle remains relaxed

33
Q

What does a-latrotoxin do, and what animal is it found in

A

triggers exocytosis of vesicles, found in black widow spiders.

34
Q

What is Lambert-Eaten Syndrome?

A

a presynaptic auto-immune disease that decrease the number of voltage gated calcium channels, so in one nerve stimulus there is less NT release

35
Q

What is Myasthenia Gravis (MG) ?

A

a common NMJ disorder of the postsynaptic. An autoimmune disorder, where there is less ACh receptors, so it takes a lot more NT to get the same effect. Antibodies bind to the AChRs, inhibiting AP initiation. There is a weakness and fatigue in facial muscles, causing droopyness.

36
Q

What are the four characteristics of skeletal muscle

A

1) Excitable
2) contract
3) Extensible
4) elastic

37
Q

What are the Na+/K+ ATPase pumps for

A

to restore the membrane potential after an AP

38
Q

What is the synaptic cleft?

A

Where the NT travels

39
Q

Alpha toxins are?

A

Blockers of nicotonic AchR
Snake venom or curare
cause paralysis as AP cant be propagated