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BMS242 - Phys/Pharm of Cells > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

Recall the divisions of a muscle from largest to smallest?

A

Muscleà Muscle Fascicle à Muscle Fibre/Cell à Myofibril à Sarcomere à Myofilaments

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2
Q

What is defined as one sarcomere?

A

The length/distance between two successive Z-lines

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3
Q

What determines the degree of contraction in muscle?

A

Degree of overlap between the actin and myosin filaments

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4
Q

What is meant by the motor unit of a muscle?

A

The motor neuron and the muscle fibre it innervates

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5
Q

One motor neuron innervates a single muscle fibre, T or F?

A

F – one motor neuron innervates several muscle fibres

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6
Q

What attribute of motor units’ accounts for the ability to finely control muscle contraction?

A

Finer control of muscle contraction comes from the motor units where one motor neuron innervates a smaller number of muscle fibres

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7
Q

A single muscle has multiple motor units, T or F?

A

T

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8
Q

Which type of postsynaptic receptor is found on muscle cells and what class of receptor is it?

A

nAchR – ligand-gated ion channel

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9
Q

The skeletal muscle action potential has a very short duration, T or F?

A

T

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10
Q

At rest the membrane potential of skeletal muscle is more positive than normal due to open CLC1 and voltage-gated K+ channels, T or F?

A

F – membrane potential is very negative

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11
Q

Which channels mediate depolarisation in the action potential?

A

Na+ channels

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12
Q

Which channels mediate repolarisation during the action potential?

A

K+ channels

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13
Q

There are different types of K+ channel that mediate the resting membrane potential and the repolarisation phase of the action potential, T or F?

A

T

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14
Q

nAchRs are Na+ ion channels, T or F?

A

F – they are cation selective but allow both Na+ and K+ through

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15
Q

Activation of the nAchRs causes depolarisation, T or F?

A

T

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16
Q

Describe the subunit composition of nAchRs?

A

Describe the subunit composition of nAchRs? nAchRs are pentameric structures consisting of 2α subunits, and 1 β, γ and δ subunit

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17
Q

What can be said about the acetylcholine binding site(s) of nAchRs?

A

There are two binding sites for acetylcholine that lie at the interface between the α and γ subunits. This means that two acetylcholine molecules have to be bound to the receptor before the ion channel opens

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18
Q

How many transmembrane domains are there in the nAchR?

A

4

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19
Q

What allows for the vast array of different nAchRs?

A

There are different types of each subunit

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20
Q

Describe the gating process of nAchRs?

A

Closed with no agonists bound à closed with one agonist bound à closed with two agonists bound à open

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21
Q

What type of disease is myasthenia gravis?

A

Autoimmune disease

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22
Q

What are the symptoms of myasthenia gravis?

A

Weakness and tiredness in the skeletal muscle

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23
Q

What is the cause of myasthenia gravis?

A

Inappropriate antibodies against postsynaptic AchRs at the neuromuscular junction that prevent acetylcholine binding

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24
Q

What difference is seen in males and females with myasthenia gravis?

A

Female age of onset in much earlier (30s) whereas in males it occurs in 60s-70s

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25
How can myasthenia gravis prove fatal?
Respiratory failure due to inability of the muscles to contract
26
Acetylcholinesterase inhibitors are used in the treatment of myasthenia gravis, how do these work?
By inhibiting acetylcholine breakdown you can prolong the effects of released acetylcholine allowing it to bind to the still functioning AchRs
27
How are corticosteroids effective in treating MG?
They are immunosuppressants that reduce levels of antibodies
28
Another treatment method for MG is using intravenous antibodies, how do these work?
They bind to the AchR antibodies and prevent them from binding to the receptors themselves
29
List two other treatment methods for MG?
Plasmaphoresis, thymectomy
30
What is meant by the muscle triad?
Structure consisting of the sarcoplasmic reticulum on both sides of a transverse tubule (T-tubule)
31
What is the purpose of the T-tubules?
Maximise the effects of the muscle action potential by allowing good spatial and temporal release of Ca2+
32
What are the T tubules?
Invaginations in the sarcolemma that allow very close proximity between the extracellular environment and the sarcoplasmic reticulum
33
The T-tubules allows Ca2+ influx very near to the actin and myosin so it can bind easily to troponin, T or F?
T
34
What type of voltage-gated Ca2+ receptors are found on the sarcoplasmic reticulum and are mechanically coupled to ryanodine receptors?
L Type Ca2+ receptors
35
The opening of voltage-gated Ca2+ channels in the sarcoplasmic reticulum plasma membrane causes opening of the coupled ryanodine receptors, T or F?
T
36
Influx of Ca2+ into the myocyte thus causes efflux of Ca2+ from the SR into the cytosol to further increase its availability for contraction, T or F?
T
37
What is myotonia?
Inherited condition characterised by hyperactivity of skeletal muscle
38
What are the main symptoms of myotonia?
Muscle stiffness, increased degree of muscle contraction and inappropriate muscle contraction
39
What is the effect on action potentials of myotonia?
Increase frequency of action potential firing in the muscles due to a rise in Ca2+ levels
40
What is meant by a myotonic seizure?
Emotional stimulus
41
What is the main trigger of a myotonic seizure?
Body wide contraction of skeletal muscle
42
There are three types of myotonia, myotonia congenita, paramyotonia and K+ aggravated myotonia, how do these differ?
Myotonia congenita is caused by a gain or loss of function mutations in a voltage-gated Cl- channel whereas paramyotonia and K+ aggravated myotonia are caused by gain of function mutations in voltage-gated Na+ channels
43
Which specific gene/ion channel is mutated in myotonia congenita?
CLC1 Cl- channel (CLCN1 gene)
44
What is Thompsen’s myotonia? What is Becker’s myotonia?
Autosomal dominant myotonia - Thompsenss //// Beckers - Autosomal Recessive
45
The ‘fainting goats of Tennessee’ are natural animal models of myotonia congenita and possess identical mutations in CLC1, T or F?
T
46
What is the role of CLC1 in setting the resting membrane potential?
CLC1 is responsible for setting the resting membrane potential. At rest it is open along with voltage-gated K+ channels. These help set the particularly negative Vm that is seen in muscle cells
47
What type of mutation in the CLC1 voltage-gated Cl- channel causes myotonia congenita?
Loss of function
48
Mutations in CLC1 tend to localised to particular regions of the protein, T or F?
F – they are scattered throughout the structure
49
What is the effect of the mutation on the function of CLC1?
Decreases the open probability of the channel meaning that the resting Vm is more positive and closer to depolarisation as less Cl- can enter the cell. This makes it closer to the threshold potential for action potential generation and thus more action potentials are fired
50
How can myotonia congenita treated?
Mexilitene (low doses) – inhibits some voltage-gated Na+ channels to block some of the action potentials in the muscle
51
What specific ion channel is mutated in Paramyotonia and K+ aggravated myotonia?
Nav1.4
52
What type of mutation leads to Paramyotonia and K+ aggravated myotonia?
Gain of function in SCN4A gene
53
What is the effect of the mutation in SCN4A on channel function?
The mutation effects the inactivation gate of the voltage-gated Na+ channel meaning that the channel stays open for longer. This allows more Na+ into the cell and thus prolonged depolarisation creating increase intracellular Ca2+ levels and thus increase muscle contraction
54
Like myotonia, the main trigger of paramyotonia is emotional stimuli, T or F?
F – the main triggers of Paramyotonia tend to be the cold or exercise
55
In myotonia congenita, there is an increase in action potential firing in the muscles whereas in Paramyotonia the action potentials generated just last for much longer, T or F?
T
56
What is the inheritance pattern of malignant hyperthermia?
Autosomal dominant
57
What are the symptoms of malignant hyperthermia?
Tachypnea, low plasma O2, high plasma CO2, tachycardia, hyperthermia (rising by 1°C/5mins), rigidity and sweating
58
What is the trigger of malignant hyperthermia?
Exposure to general anaesthetics e.g. halothane
59
What is the cause of the symptoms in malignant hyperthermia?
Uncontrolled muscle contraction
60
What causes the massive increase in body temperature seen in malignant hyperthermia?
Excessive ATP hydrolysis in order to meet increased demand by the muscles generates a lot of excess heat
61
What is the cause of malignant hyperthermia?
Mutation in the ryanodine type I receptor found on the sarcoplasmic reticulum membrane of skeletal muscle
62
What other type of channel is the mutated channel in MH coupled to?
L Type voltage-gated Ca2+ channels
63
What type of mutation causes malignant hyperthermia?
Gain in function
64
What is the effect of this mutation on the function of the affected receptor?
Increases the open probability of the RyR1 receptor in the presence of the trigger allowing for increased Ca2+ efflux from the SR and increase muscle contraction
65
How is malignant hyperthermia treated?
Dantrolene – RyR1 inhibitor that blocks the channel preventing Ca2+ efflux from the SR and alleviation of muscle contraction. This is combined with intravenous hydration, diuretics and sodium bicarbonate to counteract the acidosis
66
Tetrodotoxin is a gaunidinium neurotoxin, what are the two sources of this toxin?
Ingestion of animal containing toxin such as puffer fish, bite from animals that contain the toxin such as the blue ringed octopus
67
Tetrodotoxin itself isn’t actually produced by the animals it is found in, T or F?
T – it is produced by marine bacteria that are found in the animals themselves
68
Dangerous levels of tetrodotoxin can occurs in the nM concentration range, T or F?
T
69
What are the symptoms of TTX ingestion?
Numbness of lips and tongue, facial paraesthesia, nausea, vomiting, headaches, increasing level of paralysis
70
How do the symptoms of bites containing TTX differ from ingestion of it?
There tends to be no numbness and tingling of the lips and tongue, no facial paraesthesia
71
How can TTX be fatal?
Inhibition of respiratory muscles leading to paralysis
72
Ingestion of TTX will lead to death much quicker than a bite, T or F?
F
73
Why can't TTX toxicity be treated with antivenom?
TTX binds irreversibly to its target meaning that antibodies can't displace it
74
What is the only treatment for exposure to TTX?
Mechanical ventilation to prevent death by respiratory paralysis. This allows time for the TTX to be broken down by the body
75
Which ion channel present at the neuromuscular junction are the target for TTX?
Voltage-gated Na+ channels
76
The degree of sensitivity to TTX varies across the different types of its target ion channels, T or F?
T – some are sensitive; some are insensitive
77
How does tetrodotoxins’ effects on its target lead to its symptoms?
TTX blocks voltage-gated Na+ channels in both sensory and motor neurons. This prevents depolarisation and a reduction in neurotransmitter release. This accounts for the loss of sensation due to sensory neuron inhibition and also for the paralysis due to no postsynaptic action potentials being generated in muscles
78
TTX effects both sensory and motor neurons, which are affected first and why?
Sensory neurons are affected first hence why the initial symptoms are tingling and loss of sensation. This is due to the fact that sensory nerves are on the outside of the nerve bundles so are where the toxin reaches first
79
Explain what accounts for the varying sensitivity of different types of the target channel to TTX?
Changes in a single amino acid in the pore regions of the proteins structure is sufficient to make a voltage-gated Na+ sensitive or insensitive to TTX
80
Where are dendrotoxins found?
Venom of mamba snakes
81
Dendrotoxins are short peptides ranging from 57-60 amino acids in length, T or F?
T
82
What is the target of dendrotoxins?
Voltage-gated K+ channels
83
What is the results of dendrotoxins action on its target ion channel?
Inhibition of the voltage-gated K+ channels blocks the repolarisation phase of the action potential
84
What are the symptoms of dendrotoxin exposure?
Early weakness/numbness in the bitter extremities, drooping eyelids, paralysis of eye muscles, dysphagia, mild generalised paralysis
85
How can dendrotoxin lead to death?
Paralysis of respiratory muscles
86
How does dendrotoxin action on its target lead to muscle paralysis despite only affects repolarisation?
Results in a prolongation of depolarisation and a subsequent release of all acetylcholine from the neurotransmitter stores. This means that no neurotransmitter is available for subsequent depolarisation in the motor nerves and hence no postsynaptic action potentials can be triggered in the muscle, leading to paralysis
87
How can dendrotoxin exposure be treated?
Antivenom removes dendrotoxin already bound to voltage-gated K+ channels and also prevents any further binding of the toxin to its targets
88
What species of animal produce conotoxins?
Cone snails
89
Conotoxins have multiple targets all of which are lethal T or F?
F – conotoxins do have a wide array of targets but lethality varies significantly
90
List two different targets of conotoxins?
Voltage-gated Na+ channels and voltage-gated Ca2+ channels
91
Conotoxins block ion channel in peripheral and central nervous system that may be beneficial in blocking pain signals, T or F?
T
92
What are some of the symptoms of conotoxin exposure?
Burning pain, swelling at site, spreading numbness, cardiac and respiratory stress, loss of coordination
93
What four symptoms indicate lethal exposure to conotoxins?
Coma, stiff lips, blurred vision and paralysis

BMS242 - Phys/Pharm of Cells (3 decks)

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