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HOM > Muscles > Flashcards

Muscles Flashcards

1
Q

What makes up a motor unit

A

The presynaptic neutron and collection of muscle fibres which it innervates

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2
Q

What is the diameter of a muscle fibre generally

A

1-2 micrometer

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3
Q

How wide is a synaptic cleft

A

50-70 nm

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4
Q

What opens when an AP arrives at a presynaptic terminal?

What does this result in?

A

The motor axon opens voltage gates Ca channels

Causes vesicles to fuse with plasma membrane, releasing their contents into the cleft

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5
Q

How has vesicles fusion bee visualised

A

Using rapid freezing of the muscle during neuromuscular transmission followed by freeze fracture EM

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6
Q

What is the conc of ACh in vesicles

A

100-200mM

Roughly 10^4 molecules/vesicle

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7
Q

What is the is the release of ACh vesicles proportional to?

A

[Ca2+]^4

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8
Q

What is the mean synaptic delay?

Where does most of the delay occur?

A

1ms

Within the presynaptic terminal

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9
Q

What is the timing of ACh diffusion and post synaptic response

A

Diffusion: 10 microseconds
Response: <100 microseconds

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10
Q

ACh is an anion

True or false

A

False

It is a cation

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11
Q

What forms ACh

A

Choline and acetyl CoA by the enzyme choline acetyltransferase

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12
Q

What happens to ACh chemically when it is released?

What does it yield

A

It is hydrolysed by ACh-ase

Acetic acid and choline

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13
Q

How many subunits does a AChR channel have

How are they structured

A

5

The hydrophilic, negative side chains point inwards creating a selectivity filter which rejects anions but accepts Monovalent cations
Lipophilic point out into lipid bilayer, stabilising the pentamer
The alpha subunits each contain an extra cellular binding site for ACh

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14
Q

How was the current through a single AChR investigated?

A

Neher and Sakmann (and others) used a patch clamp

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15
Q

How long do AChR open for

What experiment was done to show this

A

<1ms

Bathed in a maintained concentration of ACh - opened in random durations

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16
Q

What is required for an AChR to open

Why is this

A

2 ACh molecules must bind to both alpha subunits

Suppressed responses to small quantities of ACh but produces a sharp response to higher concentrations

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17
Q

Should you still reread the handouts despite learning these flash cards

A

Absolutely. I have skipped entire paragraphs that Michaelmas term Joe thinks irrelevant but may later be important

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18
Q

What dictates the decay time of an end plate potential

A

Fibre diameter: the larger the fibre, the faster the decay

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19
Q

What is the reversal potential for the ESPC

A

0mV

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20
Q

Is the AChR exclusively a sodium Channel

A

No
It is a monovalent cation channel permeable to both K and Na

It is also slightly permeable to Ca

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21
Q

Do ESPCs speed up with depolarisation

Why does this occur

A

Yes due to some voltage dependence of AChR gating

It is energy efficient: if the membrane is already depolarised, the conductance switches off faster when it is no longer needed to produce depolarisation

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22
Q

What is the active ingredient in curare

A

D-tubocurarine

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23
Q

Why is curare toxic

A

D-tubocurarine competes with ACh for binding on AChR without opening the channel
This reduces the post synaptic response leading to separation of EPP and AP

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24
Q

How can the amount of ACh releases in the cleft be studied

A

Eserine blocks ACh-ase

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25
Q

What effect does eserine have

A

Prolongs EPSP and EPSCs

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26
Q

State nicotine’s relation to ACh

A

Agonist

It acts specifically on ion channel ACh receptors without activating muscarinic ACh receptors which mediate slow responses in other types of cell

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27
Q

How is snake venom deadly

A

Contains α-Bungarotoxin which binds tightly and blocks AChRs

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28
Q

How are black widows deadly

A

Their venom contains alpha-latrotoxin which produces a release of the pool of available presynaptic transmitter, resulting in a block from ACh depletion

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29
Q

How is Botulinum toxin toxic

A

Prevents release of ACh

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30
Q

What is a muscle fibre

How do they connect to bone

A

A multinucleate cell with a diameter between 50-150 microns

They are continuous with connective muscle tissue tendons which connect to bone

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31
Q

What structures directly reflect a contractile function

A

Myofibrils (made of contractile proteins that run along the fibre axis and are between 1-2 microns in diameter)

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32
Q

Are T tubules continuous with extra Elul are fluid?

A

Yep

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33
Q

What is the sarcoplasmic reticulum

A

An intracellular membrane network isolated from the extra cellular space which stores Ca ions

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34
Q

What muscles are striated

A

Cardiac and skeletal

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35
Q

In striation what is dark and what is light

A

Dark - A band containing thick filaments mainly containing myosin
Light - I band with only thin filaments, containing actin, troponin, and tropomyosin

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36
Q

Where is the Z band

A

In the centre of the I bands and provide attachment sites

The Z to Z units of myofibril form the sarcomere

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37
Q

Structure of myosin

A

1.6micrometers in length

Consists of a tail of 2 long light meromyosin strands twisted together which are both connected to globular heads

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38
Q

What does myosin bind to and what does this trigger

A

Actin

ATPase activity in the S1 fraction

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39
Q

When is the reaction between the myosin and actin permitted

A

If the tropomyosin molecule is moved deeper into the groove that is formed by the thin filaments caused when Ca binds to the troponin

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40
Q

Generally what does a cross bridge cycle do

A

Pulls the thin filaments towards the centre of the sarcomere

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41
Q

What produces sarcomere shortening

A

The relative sliding of the interdigitated thick and thin filaments

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42
Q

What does increasing myofilament overlap do?

A

Increases force generation

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43
Q

Why is there a constant isometric force at sarcomere lengths below 2.2 to 2.0 microns?

A

The middle of the thick filament lacks myosin heads, restricting opportunities for cross bridge formation, which shortens filament overlap

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44
Q

What does excessive myofilament overlap result in

What does this do

A

Thin filaments collide with one another
OR
thick filaments colliding with the Z lines

Diminish force production

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45
Q

How are cross bridges broken

A

A process that requires hydrolysis of ATP

this thus allows further cross bridge formation

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46
Q

What is rigor Mortis

A

A progressive recruitment of cross bridges that fail to dissociate

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47
Q

What 2 factors affect production of force from cross bridge cycles

A

Number of interacting sites

Force generated by each site

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48
Q

Why do muscles usually act at a disadvantage

What does this mean

A

The perpendicular distance from the line of action of the muscle to the joint is normally considerably smaller than the distance of the load to the joint

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49
Q

What does repetitive activation of of a muscle result in

What about for higher stimulation frequencies

A

A sequence of twitches with no increase in peak tensions

Muscles may be reactivated befor the previous twitch has fully recovered to result in a twitch that rises above that of a single twitch

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50
Q

What happens during tetanus

A

High activation frequencies results in tensions summing

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51
Q

Describe the length tension relationship

A

Gradual increase in tension with small degrees of stretch but beyond a certain degree of elongation there is a significantly non linear increase in tension.

After a certain length, tension decreases as length increases

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52
Q

Why does tension eventually decreases as length increases

A

Thick filaments fail to overlap so active tension cannot be developed

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53
Q

Equation for force velocity relationship

A

(F+a)(v+b)=(Fmax + a)b

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54
Q

What are smooth muscles

What is the load they work against

A

Muscles that line walls of hollow organs

The pressure within the tube

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55
Q

Shape of smooth muscle

A

Elongated and spindle shaped
NOT striated (no sarcomere)
Thick and thin are NOT transversely aligned but attached in dense bodies in the cytoplasm and to attachment plaques at the membrane
No T Tubules

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56
Q

What systems control smooth muscle

A

Autonomic (both para and sympathetic) and hormonal

Can generate active tension without nerve activity - nerves often modulate

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57
Q

What does caldesmon do

A

Binds to actin-tropomyosin to inhibit cross bridge cycling

Ca causes caldesmon to dissociate from actin by binding to the regulatory calcium binding protein calmodulin

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58
Q

How does PKC cause dissociation

A

Phosphorylates caldesmon

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59
Q

What does binding of Ca to myosin might chain do

A

Increases cross bridge formation

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60
Q

Role of myosin light chain kinase

What is this process called

A

Phosphorylation of myosin light chain causing increased cross bridge cycling which lasts until dephosphorylation by myosin phosphatase

Covalent regulation (covalent bind formed)

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61
Q

What happens if the cross bridge is dephosphorylated

A

Can maintain tension without cycling or ATP consumption

Hence why smooth muscle is >300x more efficient than skeletal in maintained contraction

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62
Q

What happens when the gut is stretched

A

Stretch activated ion channels lead to mechanically induced depolarisation and contract.
This assisted peristalsis

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63
Q

Where does an action potential travel in muscles

A

Over surface membrane and T tubule which triggers release of intracellularly stored Ca from SR

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64
Q

What is an inward rectifier and what do it do

A

A channel that Allows K to pass more easily into than out of a cell, minimising leaks and the amount of inward current required for the plateau

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65
Q

What are Ca channels responsible for in muscle

A

Plateau phase

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66
Q

What does the ryanodine receptor do

A

Acts as a calcium channel in SR

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67
Q

How many axon branches innervate a muscle fibre

Where do they attach on the muscle fibre

A

Each branch attaches to a single muscle fibre to form a motor end plate

The centre

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68
Q

How big are muscle fibres

A

1-2μm in diameter

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69
Q

How frequent are junction folds

A

Every 1-2μm

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70
Q

What are muscular active zones

A

Specialised thickenings immediately above the junction fold in the Presynaptic axon membrane

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71
Q

How big are the vesicles in muscle

Where are they found

A

50nm in diameter

Clustered around the active zone

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72
Q

What is in the synaptic cleft

A

Mucopolysaccharide glue

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73
Q

What is the basal lamina

A

A layer of extracellular material visible in EM

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74
Q

What happens as the AP reaches the motor axon

A

VG Ca channels open in the presynaptic terminal. This rise in [Ca] causes vesicles to fuse with the plasma membrane releasing their contents

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75
Q

What is the minimum synaptic delay in a frog at 17 degrees C

What is the mean

A

500μs

1ms

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76
Q

Where does most of the synaptic delay occur

How fast does ACh diffuse across the cleft and how fast is the response

A

In the presynaptic terminal

In about 10μs
<100μs

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77
Q

How is ACh synthesised

What happens after release

A

From choline and acetyl CoA
By choline acetyltransferase

It is rapidly hydrolysed by AChase which is localised to the basal lamina

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78
Q

What are the products of ACh hydrolysis

A

Acetic acid and choline

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79
Q

What is the structure of an AChR

A

4 types of gylcoprotein subunit (α,β,γ,δ) but 5 subunits total arranged ααβγδ
Hydrophilic negative side chains point into the pore creating a selectivity filter which rejects anions
The lipophilic side chains point out and stabilise the pentamer
Each α subunit contains an ACh binding site on the extracellular domain

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80
Q

What was the conductance of a single AChR

A

30pS or 30/Ω

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81
Q

What happens if AChRs are bathed in ACh

A

Openings are short <1ms and random in duration

Openings tend to be clustered into bursts with long intervals

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82
Q

What happens after a long period of maintained [ACh]?

Why does this happen?

A

The AChR stops opening or is desensitised

Protective mechanism in the case that limits the dissipation of the ion gradient in the event of catastrophic release of transmitter

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83
Q

How did Katz eliminate the AP

A

By partially blocking synaptic transmission with curare

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84
Q

What is an EPP

A

A residual subthreshold potential which rise every few miliseconds then decay (the larger the fibre diameter the larger the decay)

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85
Q

Why are EPSPs slower than EPSCs

A

The time taken to charge and discharge the membrane capacitance

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86
Q

What happens to the EPSC at more and more depolarised holding potentials

A

EPSC gets smaller and disappears at 0mV then gets larger again in the opposite direction

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87
Q

How do we know the AChR is simply a monovalent cation channel

A

The current varies linearly so the summed current varies linearly and the reversible potential is near 0mV

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88
Q

Do ESPCs change speed with depolarisation

How is this beneficial

A

Yes they speed up due to some voltage dependance of the AChR

Saves energy: if the membrane is already depolarised the conductance switches off faster when it is no longer needed to produce depolarisation

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89
Q

What does Eserine do
What is it also called
Why is it useful

A

Blocks AChase
Physostigmine
Measurement of how much ACh is released

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90
Q

What is nicotine in muscles

A

An agonist for AChRs
Works specifically on ion channels receptors without activating muscarinic AChRs which mediate slow responses in other cells

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91
Q

What does snake venom contain
Why are they bad
How have they been used

A

α-bungarotoxin
Blocks AChRs

Radioactive ones have been used to count the number of AChRs in a NMJ

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92
Q

How does black widow venom work

A

Produces a massive release of ACh in pre synaptic terminal depleting ACh stores

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93
Q

What does botulinum A do

A

Acts as an enzyme, cleaving SNAP 25 to prevent vesicle fusion with the presynaptic terminal, resulting in paralysis of the muscle.

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94
Q

How is the frequency of MEPPs affected as observed by Fatt and Katz

A

Decreased by decreasing external Ca or increasing Mg

It was increased by increasing external [K+] or osmotic pressure

These allow affect the release of vesicles

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95
Q

What did Katz suggest about vesicle release

A

1 quantum = release of 1 vesicle

Release is probabilistic: the great increase in release during an EPP would correspond to a transient increase in probability of release for the vesicle population

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96
Q

How should EPSPs fluctuate

A

Probabilistically in size but be comprised of single integral numbers of quanta

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97
Q

How to find probability of a peak

A

The area of the peak

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98
Q

Pk =?

A

(e^-m) x (m^k)/k!

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99
Q

What is m in the Poisson equation

A

Mean number of quanta released

ie quantal content

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100
Q

What can be seen if the AP is recorded near the end plate

A

The upstroke also shows the initial EPP as the membrane charges up to the threshold

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101
Q

What can you see of EPPs when curare is added to the end plate

What does this mean

A

EPPs are subthreshold and the peak size is seen to decay exponentially with distance from the end plate

The region over which a pre synaptically evoked muscle AP is limited to the area near the end plate

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102
Q

Discuss the uses of Botulinum A

A

By preventing ACh release it can be used to relax the muscles causing wrinkles in cosmetics.

However it is also the most lethal toxin known to man, causing widespread paralysis

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103
Q

Describe the action of α latrotoxin

A

forms pores to allow Ca entry resulting in vesicle release and initial stimulation, followed by depletion as continual release occurs

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104
Q

Can muscles depolarise in the absence of presynaptic activity

A

Yes - MEPP

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105
Q

At what intervals for MEPPs occur

A

Random intervals

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106
Q

What produces a MEPP

A

A quantum of about 10,000 molecules of ACh

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107
Q

Can you find depolarisation if tetrodotoxin is used to block the presynaptic APs

A

Yes: MEPPs occur despite this

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108
Q

What caused the frequency of MEPPs to change

A

Frequency decreased by a decrease in external Ca2+

Decreased with an increase in Mg

Increased by increasing external [K+] or osmotic pressure

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109
Q

What causes the frequency of MEPPs to decrease

A

Decreasing external calcium

Increasing external Magnesium

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110
Q

What causes the frequency of MEPPs to increase

A

Increasing external [K+] or osmotic pressure

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111
Q

What does a single quantum correspond with

Who showed this

A

A single presynaptic vesicle containing ACh

Katz et al

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112
Q

What dictates when an ACh vesicle is released

A

Probability

The transient increased release during an EPP is due to a transient increase in probability of release of the population of presynaptic vesicles

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113
Q

The hypothesis that quantum release is probabilistic leads to a number of predictions. Name one.

A

EPSPs should fluctuate probabilistically in size but be composed of integral numbers of quanta

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114
Q

How did Katz show the probabilistic nature of vesicle release

What did he see

A

Used low Ca2+ conditions to reduce probability of release

Distinct peaks that can be seen, reflecting the simultaneous release of 1,2,3 or 4 quanta

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115
Q

What should the area of peaks of vesicles release follow

A

The Poisson distribution

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116
Q

What is assumed when we say vesicle release follows the Poisson distribution

A

Vesicles are identical and independent

Probability of release is low

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117
Q

Give the Poisson distribution equation

Pk =?

A

(e^-m) x (m^k)/K!

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118
Q

In the Poisson distribution equation, what do each of the following stand for:

a) k
b) m
c) Pk

A

a) number of quanta
b) mean number of quanta released during an EPP
c) probability that the EPSP comprises k quanta

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119
Q

What is quanta content

A

Mean number of quanta released during an EPP

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120
Q

If we recorded the voltage near the end plate and an AP, what would we see?

How would it be different to if it were >5mm from the end plate

A

An upstroke showing the initial EPP as the membrane charges up to the AP threshold

The initial EPP disappears

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121
Q

How happens to subthreshold EPPs in a curare treated muscle

What is this due to

A

Peak size of EPPs decays exponentially with distance from the end plate

The cable properties of the muscle

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122
Q

What do the cable properties of the muscle mean

A

Without regenerative inward current through VG Na+ channels, the depolarisation fades with distance as more and more of the end plate current means out of the muscle fibre membrane

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123
Q

Why do postganglionic cells often offer dual innervation

A

They often have opposite actions

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124
Q

What do post ganglionic cells of the sympathetic nervous system release

What is its effect on cardiac muscle

A

Noradrenaline

Excitatory

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125
Q

What do post ganglionic cells release

A

ACh

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126
Q

What are the 4 ways skeletal muscle structure reflect their specialised function

A

1) myofibrils
2) internal membrane systems to regulate muscle contraction
3) specific organelles
4) abundance of myoglobin and creatine phosphate, as well as dystrophin

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127
Q

How do myofibrils directly reflect the contractile function of muscle

A

Made up of contractile proteins that run along the fibre axis

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128
Q

What are the 2 internal membrane systems in muscles that are specialised to regulate muscle contraction

A

Transverse tubules

Sarcoplasmic reticulum

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129
Q

What are transverse tubules

A

A fund network of tubes whose lamina are continuous with the ECF

Their extensive networks are placed regularly along the fibre length and transversely across the fibre axis

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130
Q

Describe the sarcoplasmic reticulum

What is the purpose

A

Forms a network of tubes and sacs whose lamina are isolated from the ECF

Intracellular storage of Ca2+

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131
Q

What organelles are particularly important in skeletal muscle cells (5)

A 
Ribosomes
Lysosomes
Lipid granules
Mitochondria
Glycogen granules
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132
Q

Why is dystrophin important

A

Abnormalities in dystrophin are associated with the pathogenesis of muscle dystrophy

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133
Q

What is the A band

A

Anisotropic

Contains thick fibres

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134
Q

What is the I band

A

The lighter isotrophic band

Contains only thin fibres

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135
Q

Where are the Z lines

A

At the centre of the I bands

These provide attachment sites

136
Q

What is the M line in muscle

A

The cross connections that alight the thick filaments

137
Q

What forms a sarcomere

A

The repeating anatomical unit of a myofibril that extends from Z line to Z line

138
Q

What are the thick proteins mostly made up of

A

Myosin

139
Q

What is a myosin molecule made of

A

A tail of 2 long light meromyosin strands that are twisted together and each tail is connected to a globular head

The head is made of a heavy meromyosin with 2 fractions (S1 and S2)

140
Q

How long is a myosin molecule

A

1.6μm

141
Q

What are the functions of the 2 fractions of the myosin head

A

S1 - contains globular heads; where ATPase activity happens

S2 - contains the necks which connect the heads to the tails

The myosin heads binds to actin, which in turn triggers ATPase activity in the S1 fraction

142
Q

What are thin filaments made of

A

Units of actin with troponin and tropomyosin

143
Q

How long are thin filaments in amphibians

A

2.05μm

144
Q

How long is the periodicity of a thin filament

A

5nm

145
Q

How are thin filaments formed

A

Each actin unit is polymerised in vivo to form thin filaments

These thin filaments are organised into paired chains that are twisted around each other with a periodicity of 36.5 nm

146
Q

Can actin bind to myosin in vitro

A

Yes

Actin is capable of binding with myosin in vitro and in vivo

147
Q

Describe the structure of tropomyosin

A

Rod shaped about 40nm long

Forms α helical subunits that become packed into the depth of the groove formed by intertwined helical actin chains

148
Q

How does a tropomyosin molecule compare to actin size wise

Why

A

One tropomyosin molecule spans 7 actin units

Prevents the binding of these actin units to myosin in resting skeletal muscles

149
Q

Physically what must happen on a molecular level to allow actin to bind to myosin

What controls this configuration change

A

Only allowed if tropomyosin is moved deeper into the groove formed by thin filaments

Troponin

150
Q

Describe the structure of troponin

A

Consists of 3 subunits: TnC, TnT and TnI

151
Q

What does the TnT subunit do

A

It is associated with the tropomyosin ribbon at 40nm intervals

152
Q

What happens to troponin when Ca2+ binds

A

Triggers a conformational changes in TnC subunit to pull tropomyosin into the actin groove

This exposes the myosin binding sites present on the actin molecule

153
Q

What is the purpose of TnI subunit

A

It is uncertain

154
Q

How does increasing filament affect force produced

A

Increases force generation

155
Q

Do myofilament lengths change

A

No

156
Q

Below what sarcomere lengths is isometric force constant

Why

A

2.2 to 2.0 microns

There are no myosin heads in the middle of the thick filaments

157
Q

How long does a single muscle twitch last

How many twitches are produced by activation from a single nerve

A

> 200ms

1

158
Q

Is there a change in peak tension if there is repetitive activation of muscle at a low frequency

A

No it simply elicits a sequence of twitches with no increase in peak tension

159
Q

Why may peak tension in muscles increase if they are repeatedly activated at a high frequency

A

The muscle may be reactivated before the previous twitch has fully recovered to result in a tension that rises above that of a single twitch

160
Q

How can tension be increased passively in muscles

A

Passively stretching a quiescent muscle

161
Q

How does tension vary as stretch increases

A

As stretch increases, tension increases gradually to a point, beyond which it increases at a faster rate

However if stretched beyond the point where thick and thin filaments don’t overlap, tension will drastically decrease

162
Q

What did AV Hill do

A

Demonstrated the inverse relationship between velocity of muscle contraction and the force generated

163
Q

What is the formula for the force velocity relationship

A

(F+a)(v+b) = (Fmax + a)b

Where a and b are constants

164
Q

When is maximum force generated

A

At isometric tension

165
Q

How much ATP is stored in cells for muscles

A

Enough for 8 twitches

166
Q

If there is only enough ATP in the cell for 8 twitches, how do we increase the amount of ATP

A

ATP is regenerated by reacting ADP and phosphocreatine (CP)

167
Q

Give the equation for the reaction of ADP and phosphocreatine

A

ADP + CP —> ATP + creatine

168
Q

CP provides an immediate backup energy supply. How much ATP can it provide for muscles

A

Enough for 100 twitches

169
Q

What is the substrate mainly utilised in muscles during intense exercise to produce ATP

A

Glucose and fatty acid (via the Krebs cycle)

170
Q

How is glucose utilised for ATP in exercise when O2 levels are low

A

Glucose is anaerobically converged to lactic acid with a limited conversion of ADP to ATP

171
Q

How can proteins contribute to ATP levels for muscles

A

Proteins can be deaminated to produce ketoacids which can act as intermediates in The Krebs cycle

172
Q

Type 1 muscle fibres have relatively high levels of aerobic enzymes. True or false?

A

True

173
Q

How do different types of muscle fibres vary in concentrations of aerobic or anaerobic enzymes?

A

Type 1: high levels of aerobic enzymes

Type 2: intermediate

Type 2b: high levels of anaerobic enzymes

174
Q

Where is smooth muscle found

What is the load on smooth muscle

A

Lining the walls of hollow organs

The pressure exerted on the walls of the hollow organ by its contents

175
Q

Do smooth muscles always have tonic activation

A

No

Some muscle like in blood vessels require tonic contraction to maintain pressure
However in the gut, phasic contraction is required to propel contents through the tube

176
Q

Which is faster at contracting: skeletal or smooth muscle

A

Skeletal

But smooth is better for sustained contraction

177
Q

Are skeletal muscles the same size as smooth muscle

A

No smooth is much smaller

178
Q

What is the shape and size of skeletal muscle

A

Spindle shaped often

Typically 3-4μm in diameter and several hundred μm long

179
Q

Why are smooth muscles smooth

A

They have no visible striations or sarcomeres in their cytoplasm

180
Q

Are thick and thin filaments arranged longitudinally in the cytoplasm it smooth muscle

A

Yes but they are not aligned transversely

181
Q

Where do filaments attach in smooth muscle

A

Dense bodies in the cytoplasm and to attachment plaques at the membrane

182
Q

Where can α actin be found

A

Attachment plaques

183
Q

Describe the T tubular system in smooth muscle

A

There is none

184
Q

Where is the SR in smooth muscles

A

There is a vesicular sarcoplasmic reticulum near the membrane

185
Q

What do gap junctions do in smooth muscle

A

Allow propagation of waves of electrical excitation between cells or transmission of intracellular messengers through the tissue

186
Q

Can smooth muscles generate active tension without nerve stimulation

A

Yes

187
Q

What is often the role of neural input for smooth muscle

A

Modulatory

188
Q

Do nerves act specifically on smooth muscule

A

No the NT released acts over a wide area of smooth muscle

189
Q

All smooth muscle is innervated by sympathetic fibres alone. True or false?

A

False

There is often dual innervation by sympathetic and parasympathetic fibres with reciprocal functions

190
Q

Is there troponin in smooth muscle

A

No

191
Q

What does Caldesmon do

A

Bonds to actin-tropomyosin thin filaments and inhibits cross bridge cycling

192
Q

How does Ca2+ affect caldesmon

A

Ca2+ causes caldesmon to dissociate from actin, promoting contraction, by binding to the regulatory calcium binding protein calmodulin

193
Q

What is the Ca. CaM and what does it do

A

The Calcium calmodulin complex

Binds to caldesmon causing it to dissociate from the thin filaments

194
Q

How else can the dissociation of caldesmon from actin be caused (other than by Ca. CaM)

A

Direct phosphorylation of PKC (protein kinase C)

195
Q

What regulates PKC

A

Diacylglycerol (DAG)

196
Q

What is DAG a product of

A

Phospholipase C activation

197
Q

How does Ca2+ directly affect myosin

A

Calcium binds directly to the cross bridge to increase cross bridge cycling

198
Q

What does the myosin light chain kinase do

How long does this effect last

A

Phosphorylates the myosin light chain to increase cross bridge cycling

This lasts until dephosphorylation by myosin phosphatase

199
Q

What activates myosin light chain kinase

A

The calcium calmodulin complex

200
Q

What kind of regulation is myosin light chain kinase phosphorylation

Why?

A

Covalent regulation

Phosphorylation forms a covalent bond

201
Q

What happens if the myosin light chain is dephosphorylated when attached to the thin filament

What is this called

A

It remains bound with high affinity

A cross bridge in this state is called a latch bridge

202
Q

What do latch bridges allow

A

The maintenance of tension without cross bridge cycling and ATP consumption

203
Q

Which is more efficient: smooth muscle or skeletal muscle?

Why is this?

A

Smooth muscle is 300x more efficient than skeletal in maintained contractions due to latch bridge formation

204
Q

What accounts for the slowness it smooth muscle contraction

A

The control of cross bridge cycling by biochemical cascades

205
Q

What indicates that the sliding filament mechanism is present in smooth muscle

A

Smooth muscle shoes a similar force-length relationship to skeletal muscle for isometric contractions

206
Q

Is contraction velocity with maximal stimulation higher in skeletal or smooth muscle

A

Lower velocity in smooth muscle

207
Q

How can velocity of shortening be increased in smooth muscle

A

Increased levels of cross bridge phosphorylation

208
Q

Is lots of phosphorylation required for maximum isometric force generation in smooth muscle

A

No

209
Q

What happens to calcium and the rate of cross bridge phosphorylation in a sustained contraction

A

Calcium and the rate of cross bridge phosphorylation increase to a peak initially to produce rapid shortening and the subsidise to lower levels while tension is maintained

210
Q

Name 3 organs which have smooth muscle that contacts phasically in response to stretch

A

Bladder
Uterus
Gut

211
Q

What causes smooth muscle phasic contraction in response to stress in organs like the bladder

A

Mechanically induced depolarisation due to stretch activated ion channels in the muscle membrane

212
Q

What does tonic stretch induced contraction allow

A

Compensative adjustment of tension to keep length constant

213
Q

In cardiac and skeletal muscle how is calcium mediated

A

Through its binding to the TnC subunit of troponin

214
Q

How many calcium binding sites are on a skeletal TnC subunit

Which binding sites are special

A

4

2 of the sites have a much higher affinity for Ca2+ than Mg2+ and are critical sites for regulation of cross bridge activation

215
Q

Is the T tubule extracellular space

What does this mean

A

Yes

The total surface area is 6-10x larger than that of a sarcolemmal cylinder alone

216
Q

Where are the T tubule networks found

A

Between the A and I band in mammalian skeletal muscle

In the Z band in amphibian skeletal muscle and mammalian cardiac muscle

217
Q

What is the terminal cisternae

A

Where the sarcoplasmic reticulum comes into a close relationship with the T tubules

218
Q

How are the SR and terminal cisternae arranged

A

The membranes or 2 membrane systems come into close proximity where 2 terminal cisternae sandwich a T tubule

This gives rise to a triad arrangement

219
Q

How much of the tubular surface is triadic regions

A

70% (in frog muscle)

220
Q

What happens when the tubular membrane in muscle is depolarised

A

It triggers release of intracellular calcium from the SR, elevating free cytosolic calcium concentration

This activates contractile proteins and initiates mechanical activity

221
Q

What is the stimulation frequency required for tetanus is

a) slow muscle
b) fast muscle

A

a) 40 per second

b) 300 per second

222
Q

Which ion channel is particularly common in muscles cell membranes

Are they equally popular on the tubular surface

A

Sodium

No they are less common there

223
Q

How many types of potassium channels are there in nerve and muscle

A

1 type predominates in nerve

There are at least 3 types of K channel in muscle

224
Q

Are inward rectifying K channels found in muscle

A

Yes

225
Q

What are the 3 types of K channel in muscle

A

One is activated by depolarisation over a time course similar to that in nerve membranes

One is activated over a considerably longer time course of hundreds of ms

The final type is an inward rectifying K channel

226
Q

What is the purpose of the muscle’s inward rectifying K channel

A

Minimise leak currents to reduce the amount of inward current required to sustain the plateau phase of cardiac APs

227
Q

How does the resting skeletal muscle cell differ from a nerve cell in terms of conductance

A

Resting skeletal muscle shows a significant chloride conductance

228
Q

What is the point of the Cl- conductance I’m resting skeletal muscle

A

Important in stabilising membrane potential between episodes of electrical activity

229
Q

What is myotonia congenita

A

A deficiency of functioning Cl- channels in skeletal muscle which leads to unwanted repetitive AP firing

230
Q

What are responsible for the inward currents that give rise to the regenerative activity in invertebrate muscle

A

Ca2+ channels

231
Q

What phase of the cardiac AP is Ca2+ responsible for

A

The plateau phase

232
Q

What may abnormalities associated with calcium permeability lead to?

A

Pathological changes in dystrophic muscle

233
Q

What is important about fact that the T tubule lamina constitute a restricted extracellular space

A

Ions can accumulate or be depleted from here as diffusion with the rest of the ECF is v slow

234
Q

What is excitation contraction coupling

A

The series of events that connect membrane depolarisation with myofilament activation

235
Q

The T tubules are capable of only passive electrical conduction. True or false?

A

False

They themselves can also propagate action potentials

236
Q

Are t tubules important in excitation - contraction coupling?

A

Yes they play a vital role in initiating and synchronising contractile activity through the entire cross section of muscle fibre

237
Q

What does excitation contraction coupling begin with

A

The detection of the T tubular membrane depolarising by a voltage sensor

238
Q

What is a voltage sensor

A

A modified calcium channel protein located in the tubular membrane of muscle

Its configuration varies steeply with membrane potential

239
Q

What causes the voltage sensor to change conformation

What does this change lead to

A

Charge movements

Release of Ca2+ into the cytosol from the SR

240
Q

In skeletal muscle, what does elevated cytosolic calcium reflect?

A

It almost entirely reflects the release from the SR (there is v little influx from the ECF)

241
Q

In skeletal muscles where does the transduction of Ca2+ from the SR to cytoplasm occur

Why do we think this

A

At the triad

EM studies show foot processes joining the cisternae and tubular membranes in the triad complex.

242
Q

What are the foot processes in the triad thought to be

A

Cytoplasmic components of the ryanodine receptor

243
Q

Where are the intracellular portions of the ryanodine receptor found

What does this portion receptor act as?

A

Within the SR membrane

A calcium channel,
the cytoplasmic portion makes up most of the foot process

244
Q

What are the foot processes on the SR close to

A

Structures embedded in the T tubule membrane, thought to be voltage sensors

245
Q

How are changes in polarisation in the T tubule connected to the SR

A

Direct mechanical coupling between the ryanodine receptors and voltage sensors

246
Q

What is the result of the coupling of the ryanodine receptors and the voltage sensors on the T tubule

A

The release of intracellular Calcium ultimately initiates mechanical activity through their binding to troponin

247
Q

What is malignant hyperthermia

A

A genetic defect of the ryanodine receptor resulting in muscle spasms and excessive heat generation

248
Q

What are the clinical manifestations of malignant hyperthermia usually triggered by

A

Halothane (a common general anaesthetic)

249
Q

How is Ca re-sequestered after activation

A

Active transport of Ca2+ into the SR by a membrane Ca-ATPase

250
Q

Where is the Ca-ATPase found

A

In the longitudinal regions of the SR membrane, remote from the terminal cisternae

251
Q

Describe the Ca-ATPase molecule

A

Molecular weight of 100kD

Transports 2 Ca2+ for each molecule of ATP hydrolysed

Pumps calcium from the cytosol to SR, building up a thousand fold concentration gradient across the membrane

252
Q

Is the Ca2+ just floating around in the SR

A

NO

a number of intra-luminal proteins sequester the luminal Ca2+
Eg calsequestrin

253
Q

Name a luminal protein that sequesters luminal Ca2+

Describe it

A

Calsequestrin

Has a 1:45 binding ratio for Calcium
Occurs most abundantly in the terminal cisternae lumina

254
Q

Why is sequestering required in the SR

A

To return cytosolic calcium concentration to levels below those required for significant troponin binding thereby ending the twitch

255
Q

How big are cardiac muscle cells compared to skeletal muscle cells

A

Cardiac muscle cells are significantly shorter (~10 microns in diameter and 200 microns in length)

256
Q

How are cardiac muscle cells linked

A

They are linked in a branched and end to end fashion by intercalated disks, producing a syncytium

257
Q

Does the syncytium in cardiac muscle cells conduct electrical or mechanism a forces between component cells?

A

Both

258
Q

At the ultrastructural level, cardiac muscle resembles which other muscle type

How are they similar and different

A

Skeletal

Both have a SR and T tubule system

Cardiac SR is less developed
The SR - T tubule complex is a dyad in cardiac but a triad in skeletal

259
Q

What are the different functions of different types of cardiac muscle

A

Contractility
Or
Impulse conduction/
Impulse generation

260
Q

Where are the cardiac muscle cells specialised for impulse conduction/ generation found?

A

SAN
AVN
Bundle of His

261
Q

Give an overview of a cardiac action potential

A

There is an initial rapid depolarisation but then after the early overshoot, the ventricular membrane potential falls quickly to 0mV and remains here in a plateau

262
Q

What are the 5 phases of ventricular action potential

A

Phase 0= very rapid depolarisation
Phase 1= initial Brief rapid repolarisation
2= the plateau
3= terminal repolarisation to Restore membrane potential to its resting potential
4= electrical diastole

263
Q

What causes the initial rapid rising phase of an AP in cardiac muscle

A

The opening of Na channels

264
Q

In cardiac muscle, what initiates excitation contraction coupling

What follows this

A

Prolonged inward Ca2+ currents

This produces a long lasting plateau phase

265
Q

Where is the plateau phase in cardiac muscle particularly prominent

A

In the Purkinje and ventricular fibres

266
Q

How long can a plateau phase be

A

Up to 500ms after the early upstroke

267
Q

Does verapamil do

Name a similar drug

A

Blocks calcium channels, diminishing the amplitude of the plateau phase

Nifedipine

268
Q

Discuss membrane resistance during the plateau phase

A

Membrane resistance is increased in the plateau phase as a result of inward rectification brought about by K channels at such voltages

269
Q

What do inward rectifiers do during the plateau phase

A

Reduces inward current what would otherwise be required to hold the membrane potential at plateau level

This ultimately minimises the dissipation of calcium concentration gradients across the cell membrane

270
Q

What does the repolarisation of cardiac APs result from

A

The gradual activation of further potassium channels

The outward current drives the membrane towards the resting level

271
Q

How do APs adjust to heart rate

Why is this

A

The AP duration appears to adjust inversely to heart rate

To allow appropriate adjustment of the relative durations of systole and diastole in relation to changes in the interval between successive APs

272
Q

What is the primary pacemaker

Why

A

SAN

These are the cells whose resting potential drifts towards the threshold at a faster rate

273
Q 
How often does the 
a) SAN
b) AVN
c)  Purkinje fibres 
discharge
A

a) 60-80 times/min
b) 40-60
c) 30-40

274
Q

When do the AVN or Purkinje fibres take over control of heart rate

A

These are secondary pacemakers so take over when there is severe SAN inhibition

275
Q

Which contractile cardiac muscle cells produce pacemaker activity

A

cardiac muscle cells whose main function in contractile don’t usually produce pacemaker activity

276
Q

What is the normal human heart beat frequency

How do the SAN cells maintain this

A

70 beats per minute

The membrane of SAN cells have a high background leak conductance that results in intrinsic firing

277
Q

What does the SAN’s pacemaker role dictate

A

The rate and sequence of activation of different regions of the heart

278
Q

When may the SAN function be abnormal

A

Sick sinus syndrome

279
Q

What may cause congenital sick sinus syndrome

A

A mutation of the gene responsible for the formation of the α subunit of SCN5A (a sodium channel)

280
Q

What does the AV ring do

A

Electrically isolates the ventricles from the atria - the AVN provides the only communication between them

281
Q

What is the role of the AVN when the SAN works just fine

How does it perform this role

A

To synchronise the sequential atrial and ventricular contractions

Conduction through this node is slower (0.2 m/s) than through the remaining myocardium

282
Q

Do cells in cardiac conducting tissues like the Bundle of His have myofilaments?

A

Yes but they have fewer, instead they show faster impulse generation and propagation than surrounding myocytes

283
Q

What is the difference in conduction speed between His cells and normal cardiac myocytes

A

His: 2-5 m/s
Myocytes: 1m/s

284
Q

What are the left and right bundle branches

Which is smaller

A

Two fans formed by the bundle of His immediately distal to the AVN

The right is smaller and the left divides into anterior/ superior and posterior/ inferior fascicles

285
Q

What is the importance of the fascicles from the left bundle branch in the heart

A

Impulses from the AVN are conducted through the fascicles to the apex of the ventricles. Impulses are then propagated through surrounding myocardium at a slower rate.

286
Q

What does the pattern of electrical conduction from the bundle branch fascicles result in

A

A ventricular contraction that optimises extrusion of blood as contraction begins at the apex and spreads to the base of the ventricles

287
Q

When is cardiac muscle in the absolute refractory period

Why is this

A

I’m between the early rapid depolarisation to the point where the membrane potential is repolarised to ~-40mV

Inactivation of fast Na+ channels

288
Q

When is the cardiac muscle in relative refractory period

A

From ~-40 to ~-80mV (complete repolarisation)

289
Q

What happens to action potentials in cardiac muscle during the relative refractory period

A

Evoked APs have smaller amplitudes and rate of rise is conducted more slowly

290
Q

How long is the relative refractory period

A

It is proportional to the duration of the action potential

291
Q

order the following based on length of refractory period, from smallest to largest:

Ventricular, atrial, Purkinje fibre

A

Atrial< ventricular < Purkinje

292
Q

Refractory period is directly proportional to heart rate. True or false?

A

False

The refractory period is inversely proportional to heart rate

293
Q

a) Why do we have a longer refractory period on the heart

b) What would happen without this

A

a)To ensure the heart pumps rhythmically at appropriate intervals
The duration of the refractory period in a normal heart allows the impulse from the SAN to propagate throughout the entire myocardium just once

b) re-entry arrhythmia would occur

294
Q

How can re entry arrhythmia be treated

A

By lengthening the refractory period by pharmacological means

295
Q

Is tetanus possible in the heart?

Why is this?

A

No the refractory period is too long

It would be detrimental to heart function, in contrast to the situation in skeletal muscle

296
Q

What is the resting potential of smooth muscle

A

-50 to -70mV

297
Q

Name organs where you may get smooth muscle showing slow AP firing

A

Vas deferens

Uterus

298
Q

Name organs where you may get smooth muscle showing plateau potentials

A

Stomach

Ureter

299
Q

Name an organ where you may get smooth muscle showing rhythmic oscillations in membrane potential

A

Intestine

300
Q

What is the effect or tetrodotoxin on smooth muscle

A

Tetrodotoxin does not block smooth muscle spiking activity as it is produced by VG Calcium channels

301
Q

What is the important of the higher surface area to volume ratio in smooth muscle compared to skeletal muscle

A

For smooth muscle, it makes the entry of external calcium more important whereas Ca2+ release from the SR is more important in skeletal

302
Q

What initiates mechanical activity in cardiac muscle

A

Increased [cytosokic Ca2+] following membrane depolarisation, resulting in calcium binding to troponin

303
Q

How many calcium binding sites in cardiac troponin

A

3

304
Q

What is the most important source of activator calcium in cardiac muscle

A

From the SR in response to T tubule depolarisation

305
Q

Why is extracellular calcium still important in the heart

A

Calcium entry provides the stimulus from calcium release from the SR

Thus doubling extracellular calcium will nearly double maximum cardiac contractile force

306
Q

Give 3 differences between the mechanical activation of skeletal and cardiac muscle

A

1) amount of calcium released
2) how they modulate the strength of contraction
3) the effect of calcium influx

307
Q

How does the amount of calcium released on activation differ between skeletal and cardiac muscle

A

In skeletal the release of intracellularly stored calcium is well in excess of that required fro maximal contraction

In cardiac, the amount of intracellular calcium released is not supramaximal but is closely influenced by factors which influence inotropy

308
Q

How does skeletal muscle modulate contractile strength

A

By varying recruitment of activated fibres

309
Q

How does cardiac muscle vary strength of contraction

A

Intercalated disks link all muscle in a syncytium so all muscles cells must be activated. Therefore the strength of contraction is regulated by the amount of Calcium made available

310
Q

How are cytosolic calcium levels maintained in cardiac muscle between APs

A

Both surface and SR membranes have calcium ATPase pumps which move Ca2+ into the ECF or SR lumina

Sodium - calcium exchange drives efflux of calcium across the surface membrane

311
Q

How does the Ca - Na pump work in cardiac muscle

A

It utilises the energy from the influx of Na down the electrochemical gradient, which was established by a Na/K pump

312
Q

How does digitalis and other cardiac glycosides work

A

Used in management in cardiac failure

They block the Na/K pump so intracellular sodium increases, decreasing its electrochemical gradient, making it harder for the Ca/Na exchanger to remove Ca

Intracellular calcium builds up, increasing contractile force

313
Q

The passive tension-length relationship is much steeper in cardiac muscle than skeletal. True or false?

What does this mean

A

True

Even resting cardiac muscle is considerably more resistant to stretch than skeletal

314
Q

Active shortening of cardiac muscle takes place on what part of the passive length tension curve

A

Almost entirely on the part where increased stretch leads to increased contractile force

315
Q

What law may the steep passive length- active tension relationship of cardiac muscle explain

A

The Frank Starling Law

316
Q

Which 2 ways make the heart a self regulating pump thanks to the Frank Starling Law

A

Both with respect to demands from the peripheral circulation and in balancing the pumping by the left and right sides of the heart

317
Q

What is the Bowditch effect

A

When myocardial contractility increases with heart rate

318
Q

What is the Anrep effect briefly

A

Myocardial contractility increases with afterload

319
Q

Which neurotransmitter slows heart rate

How does it do this

A

ACh

Increases membrane K conductance which hyperpolarises the membrane of the SAN during diastole

320
Q

Which neurotransmitter reduces cardiac contractility

How

A

ACh

By resting the low inward calcium current

321
Q

Name 2 sympathetic transmitters of the heart

A

Noradrenaline

Adrenaline

322
Q

How do noradrenaline and adrenaline increase heart rate

A

They increase the rate of pacemaker depolarisation during diastole and in hyperpolarisation early in diastole

Also increase inward calcium current that contributes to the inotropic effect exerted by catecholamines on cardiac function

323
Q

What does the action potential look like after the effect of adrenaline

A

Shows a higher but shorter plateau

324
Q

What does the ECG waveform record

A

The changes with time in potentials in the body surface caused by changes in the summated cardiac polarity brought about by electrical events in the myocardium

325
Q

What does a positive deflection on an ECG generally denote

A

Generally when a depolarising impulse is conducted towards the electrode or if a repolarisation wave is propagated away from the electrode

326
Q

Why are atrial deflections on an ECG smaller

A

They have smaller muscle mass

327
Q

The P wave is equivalent to an atrial QRS complex. True or false?

A

True

328
Q

How big should a P wave be

What if it is bigger than this

A

<0.12s wide and <0.3mV high

Suggests atrial enlargement

329
Q

What should the PQ interval look like

What if it is not

A

Should be consistent and between 0.12 and 0.24s

If too short: accessory pathways present
If too long: diagnostic of first degree heart block

330
Q

What should the QRS complex look like

What if it doesn’t

A

<0.12s

If too long: intraventricular conduction defect, including left and right bundle branch block

The sum of deepest QS and tallest R <3.5mV
If greater than this: left ventricular hypertrophy

331
Q

What is the cardiac cycle length

A

RR or PP

332
Q

How long should the QT interval be

But

A

Less than 0.45s

But it is frequency dependent

If too long: Long QT Syndrome (may be secondary to drug treatment)

333
Q

The ST segment is usually isoelectric with normal QRS complex. True or false

A

True

334
Q

What are the 3 major diagnostic categories for which the ECG is useful

A

Conduction disorders
Rhythm disorders
Disorders of Myocardial metabolism

335
Q

Discuss disorders or rhythm

A

Arrhythmias May originate in the atria (better tolerated) or in the ventricles

Result in disrupted PQRST sequence

336
Q

When does the muscle relax

A

When calcium influx stops

337
Q

Other than VG calcium channels, what are other sources of intracellular calcium elevation ?

A

Receptor-operated calcium permeable channels mediate calcium influx (these are activated by hormones or NTs)

PLC catalysed formation of IP3 from PIP2. IP3 opens calcium channels in the SR

HOM (11 decks)

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