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Nerve & Muscle > Neuromuscular Junction > Flashcards

Neuromuscular Junction Flashcards

1
Q

What is a motor unit?

A

The motor neurone and all of the skeletal muscle fibres that are innervated by that motor neurone’s axon terminals

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2
Q

What happens when the motor neurone of a motor unit fires?

A

All of the muscle fibres within the motor unit will contract together

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3
Q

How does the size of the motor unit influence the type of control required?

A

For a forceful contraction there are more nerve endings innervating more muscle fibres

When fine control is required there are less nerve endings and less muscle fibres are innervated

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4
Q

What is the role of gap junctions in the motor unit?

A

There are no gap junctions between muscle fibres

The action potential does not spread between them

Contraction is caused by direct innervation

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5
Q

Why is neuromuscular transmission 1:1?

A

Every presynaptic action potential will result in one postsynaptic potential

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6
Q

Why is neuromuscular transmission a unidirectional process?

A

It only happens in one direction

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7
Q

What is the time delay in neuromuscular transmission and why is there a delay?

A

Inherent time delay of 0.5 to 1 milliseconds

Due to the action potential being transferred from the nerve to the muscle

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8
Q

What is the neuromuscular junction?

A

It is a specialised region that is found at the synapse between motor neurones and skeletal muscle fibres

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9
Q

Where are the neurotransmitter vesicles found?

A

They are inside the terminal bouton

They are lined up directly above structures on the postsynaptic cell called postjunctional folds

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10
Q

What are postjunctional folds?

A

Regions where the neurotransmitter receptors are concentrated

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11
Q

Where are motor neurone cell bodies found within the spinal cord?

A

Inside the ventral horn

They send out axons via ventral roots to innervate appropriate muscles

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12
Q

How do the motor neurones change in composition as they reach muscle fibres?

A

The axons of motor neurones are myelinated as they pass through the CNS and into the peripheral nerves

They divide to supply thin unmyelinated fibres

Each fibre can innervate several individual muscle fibre cells

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13
Q

Where in the neurone does neurotransmission occur?

A

Each axon terminates in a terminal bouton

The nerve is 50 nm above the muscle and does not come into direct contact with it

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14
Q

What is significant about the bouton shape?

A

It gives a large surface area for neurotransmitter release

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15
Q

What happens when the action potential reaches the terminal bouton?

A

It causes depolarisation of the presynaptic membrane

Depolarisation causes voltage-gated calcium channels to open

There is an influx of Calcium ions

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16
Q

What is the role of microdomains in chemical transmission?

A

Increase in Ca2+ concentration can trigger many different cellular cascades

We only want vesicles to be released

Microdomains ensure the increase in Ca2+ is localised to the area around the vesicles

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17
Q

What happens in chemical transmission when calcium ions enter the bouton?

A

They cause the fusion of neurotransmitter vesicles with the presynaptic membrane

The neurotransmitter is released by exocytosis into the synaptic cleft

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18
Q

What happens after acetylcholine is released into the synaptic cleft?

A

Acetylcholine will bind to nicotinic receptors on the muscle cell membrane

Nicotinic receptors are activated allowing Na+ to enter the muscle cell and cause membrane depolarisation

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19
Q

Why are vesicles within the synaptic terminal lined up directly above post-junctional folds?

A

The post-junctional folds are on the postsynaptic membrane

The neurotransmitter receptors are concentrated here

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20
Q

Why are some vesicles held back in reserve?

A

Vesicles are pre-docked and lined up in an ordered way

The ones in reverse will come forward to replace the docked vesicles as they release their content

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21
Q

What is the basal lamina and what is its role in the synaptic cleft?

A

It is a layer of extracellular matrix that is secreted by epithelial cells

It provides support within the synaptic cleft

Acetylcholinesterase is attached to the basal lamina

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22
Q

Why is the nicotinic receptor described as heteromeric?

A

It is made from 5 subunits and each subunit is of a different molecular type

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23
Q

Why are there nicotinic receptors with different characteristics?

A

The exact combination of numerous subunit types and subtypes will differ in different tissues

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24
Q

How many subunits make up a nicotinic receptor?

A

5 subunits

Each subunit forms 4 transmembrane spanning segments

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25
Q

How is the nicotinic receptor activated?

A

The 2 alpha subunits have ACh binding sites

2 molecules of ACh must bind to the receptor before it is activated

Binding of ACh allows the central ion pore to open

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26
Q

What is one quantum?

A

The contents of one synaptic vesicle

Around 5,000 molecules of acetylcholine

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27
Q

How many receptors are activated by one vesicle of ACh?

A

Release of acetylcholine from one vesicle can activate 1,000 - 2,000 receptors

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28
Q

What is a miniature end plate potential?

A

It is the depolarisation produced by a single quantum of acetylcholine

This causes a local depolarisation of 0.5 mV

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29
Q

What is meant by a MEPP being produced randomly?

A

It can be produced without an action potential or calcium influx

You cannot get parts of a quantum released, only multiples of one

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30
Q

How do end plate potentials arise from MEPPs?

A

MEPPs have an additive effect

They become EPPs when the action potential causes the release of many vesicles

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31
Q

How does an EPP lead to an action potential?

A

When EPPs cause the membrane to reach the threshold value, voltage-gated ion channels in the postsynaptic membrane will open

There is an influx of sodium ions

The action potential leads to muscle contraction

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32
Q

How is acetylcholine broken down after depolarisation of the postsynaptic cell?

A

It dissociates from the receptor when it is hydrolysed by acetylcholinesterase

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33
Q

What is ACh broken down into?

A

Acetylcholine is hydrolysed into acetate and choline

The synaptic knob reabsorbs choline from the synaptic cleft

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34
Q

How is acetylcholine synthesised?

A

Acetate reacts with co-enzyme A to form acetyl-CoA

Acetyl-CoA reacts with choline to form acetylcholine

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35
Q

How is choline transported into the neurone?

A

It is derived from the diet

It is taken up by the neurone through a sodium-dependent choline transporter

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36
Q

Where does acetyl-CoA come from?

A

It is synthesised from glucose and/or fatty acids during the Krebs cycle

37
Q

Why does ACh synthesis take place in the cytoplasm?

A

There are choline acetyl-transferase enzymes in cholinergic neurones

38
Q

Which ion is needed to concentrate ACh into vesicles?

A

ACh being concentrated into vesicles is coupled to the counter transport of H+

39
Q

Why is H+ needed to concentrate ACh into vesicles?

A

The sodium-dependent ACh transporter is a cotransporter

It moves H+ down a CG out of the vesicle

A molecule of ACh is transported into the vesicle

40
Q

Why is concentrating ACh into vesicles an energy dependent process?

A

The creation of the H+ gradient is an active process

41
Q

What is the role of synapsin?

A

Reserve vesicles are anchored near the active zone by synapsin

Synapsin tethers the reserve vesicles to actin filaments

42
Q

Why does docking of vesicles occur?

A

When the v-Snare protein on the vesicle binds to the t-Snare on the membrane at the active zone

43
Q

What happens to the products of ACh breakdown?

A

Choline is taken up into the nerve terminal by cotransport with Na+

Acetate is excreted as a waste product as it is broken down to water and carbon dioxide

44
Q

What happens to the vesicles after the ACh has been released?

A

They become part of the membrane through endocytosis

They become clathrin coated and internalised

The vesicle fuses with the endosome leading to the production of new vesicles through budding

45
Q

Why is neuromuscular block used clinically?

A

It is used as a supplement to anaesthesia to produce paralysis

46
Q

What is a problem with giving the appropriate dose of neuromuscular-blocking drug?

A

It may paralyse the muscles required for breathing

Mechanical ventilation should be available to maintain adequate respiration

47
Q

What is Tubocurarine?

A

It is a non-polarising competitive nAChR antagonist

48
Q

How does a non-polarising competitive nAChR work?

A

It competes with ACh for the binding sites on the nicotinic receptor

This causes muscle paralysis to occur gradually

49
Q

How is Tubocurarine counteracted?

A

Paralysis can be overcome by increasing ACh concentration

Acetylcholinesterase is inhibited to achieve this

It is a competitive drug

50
Q

How does Tubocurarine affect the motor end plate?

A

It does not depolarise it

51
Q

What happens if small and large doses of Tubocurarine are given?

A

At small clinical doses it predominantly acts on the nicotinic receptor to block binding of ACh

At higher doses is can block pre-junctional Na+ channels

This will decrease ACh release

52
Q

What are the side effects of Tubocurarine and why?

A

Hypotension and bronchospasm

It increases histamine release which is a vasodilator

53
Q

What is a therapeutic use of Tubocurarine and what is its time of onset and duration of action?

A

It is used in surgery

It has a slow onset of < 5 mins

It has a long duration of action of around 30 mins

54
Q

How many ACh receptors need to be blocked for neuromuscular conduction to fail?

Why does it fail?

A

70-80% of receptors need to be blocked

EPPs can still be detected but they are too small to reach the threshold potential needed for activation of muscle fibre contraction

55
Q

What is Succinylcholine?

A

A depolarising nAChR agonist

56
Q

How do depolarising nAChR agonists work?

A

They depolarise the motor end plate

This causes persistent depolarisation of the neuromuscular junction

57
Q

What are the 2 phases of persistent depolarisation of the neuromuscular junction?

A

Phase I - depolarisation

Phase II - desensitising

58
Q

What happens during the depolarisation phase caused by Succinylcholine?

A

The membrane is depolarised by opening nAChR channels

Causes a brief period of muscle fasciculation (twitching)

After sufficient depolarisation has occurred, phase II sets in

59
Q

What happens during the desensitising phase caused by Succinylcholine?

A

End plate eventually repolarises

Succinylcholine is not metabolised as quickly as ACh so it continues to occupy the receptor

The muscle is no longer responsive to ACh

Full neuromuscular block is achieved that leads to flaccid paralysis

60
Q

When is Succinylcholine used and what is the adverse effect?

A

It is used in surgery

It is short acting so is given continuously through IV

If it is administered with halothane, genetically susceptible people will experience malignant hyperthermia

61
Q

What are Neostigmine and Edrophonium?

A

Cholinesterase inhibitors

62
Q

How do cholinesterase inhibitors work?

A

They inhibit acetylcholinesterase

This prevents the breakdown of ACh so the level and duration of action of ACh is increased

63
Q

What is the main use of Neostigmine?

A

Treatment for myasthenia gravis

It increases neuromuscular transmission

64
Q

What is the main use of Edrophonium?

A

Diagnosis of myasthenia gravis

65
Q

What are other uses of cholinesterase inhibitors?

A

They are an antidote for non-depolarising blockers such as Tubocurarine

Treatment for glaucoma

Treatment of postural tachycardia syndrome

66
Q

How do cholinesterase inhibitors have adverse effects on other parts of the body?

A

They do not only act on nicotinic receptors

They also act on receptors on the muscles that respond to ACh

67
Q

How do cholinesterase inhibitors act on the parasympathetic nervous system?

A

They can cause abdominal cramping, diarrhoea, salivation and incontinence

68
Q

Why are cholinesterase inhibitors used in insecticides and weapons?

A

They act as nerve agents

They are stable, easily dispersed, highly toxic and have rapid effects through the skin or via respiration

69
Q

What are the immediate symptoms of nerve agents?

A 
runny nose
watery eyes
drooling
constriction of pupils
eye pain
difficulty breathing
confusion
muscle weakness
70
Q

How do nerve agents usually cause death?

A

Asphyxia due to the inability to control muscles involved in breathing

It can cause death within 1 to 10 minutes

71
Q

What is atropine used for?

A

It is an antidote used for nerve agents

72
Q

What do tetanus and botulinum toxins do to the NMJ?

A

They reduce the probability of neurotransmitter release

They prevent vesicles from binding to the pre-synaptic membrane

73
Q

How do botulinum toxins work?

A

It cleaves SNARE proteins that are involved in fusing synaptic vesicles to the plasma membrane

Cleavage of SNARE proteins inhibits ACh release

74
Q

What does Tetrodotoxin do to the NMJ?

A

It binds to muscle Na+ channels to block activation

This prevents presynaptic terminal depolarisation and affects the amount of ACh released

75
Q

What is Lambert-Eaton syndrome?

A

A presynaptic condition that leads to reduced ACh release

It is a rare autoimmune response that inhibits Ca2+ channels in the presynaptic membrane

76
Q

Why does Lambert-Eaton syndrome affect muscles?

A

There is no calcium influx so there is a reduced probability of vesicle release

When no ACh is released, there is no muscle contraction

77
Q

How is Lambert-Eaton syndrome usually characterised?

A

Fatigue, weakness in limb muscle groups, autonomic dysfunction and abnormal reflexes, dry mouth

Does not usually affect respiratory, facial or eye muscles

78
Q

What age group is Lambert-Eaton syndrome usually observed in?

What do most of these patients suffer from?

A

It is usually observed in middle aged and older individuals

About half of the patients will have a small cell lung cancer

79
Q

How is Lambert-Eaton syndrome diagnosed?

A

Electromyography

This involves applying electrical impulses to nerves and measuring the electrical response of the muscle

80
Q

After a suspected diagnosis, what techniques are used to confirm Lambert-Eaton syndrome?

A

Often symptoms are worse in the morning

Chest x-rays are used for possible lung malignancy

Antibodies are used to look for Ca2+ channels

81
Q

How is Lambert-Eaton syndrome treated?

A

If there is an underlying malignancy, treatment will resolve the symptoms

Immunosuppressants such as corticosteroids are used

Amifampridine is used

82
Q

How does Amifampridine work?

A

It blocks potassium ion channels

This increases the duration of the action potential so more ACh is released

83
Q

What is myasthenia gravis?

A

It is a postsynaptic disease that involves an immune response against nicotinic receptors

If there are no receptors, the NMJ is less responsive to the ACh that is released

84
Q

What are the symptoms of myasthenia gravis?

A

Muscle weakness and fatigue

85
Q

What are the 2 forms of muscles that myasthenia gravis affects?

A

Extraocular muscles which control movement of the eye and eyelid elevation

Generalised muscle weakness due to repetitive stimulation decreasing contractile strength

Weakness is greatest at the end of the day or after exertion

86
Q

How does decreasing the number of AChR affect postsynaptic muscle fibres?

A

There are fewer AChRs to bind to so the EPPs are smaller

Smaller EPPs means less chance of the postsynaptic muscle fibres being activated

87
Q

How is Myasthenia Gravis diagnosed?

A

MRI or CT scan for possible thyoma

Antibodies to ACh receptor

Electromyography

Edrophonium OR Neostigmine test

Often symptoms will improve upon rest

88
Q

How is Myasthenia Gravis treated?

A

Treatment is directed at enhancing transmission

Anticholinesterase

Immunosuppressants such as corticosteroids

Some patients have a tumour of the thymus and removing it leads to improvement

89
Q

How does the age at which men and women are usually affected by myasthenia gravis vary?

A

Women afflicted at an early age with hyperplasia of the thymus

Men are affected at an older age with cancer of the thymus

Nerve & Muscle (5 decks)

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