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Semester 2 > M&R Session 5 > Flashcards

M&R Session 5 Flashcards

0
Q

What happens at the nerve terminal?

A

Depolarisation –> opens V-G calcium channels –> calcium influx –> release of neurotransmitter

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1
Q

Which channels are found in the nerve terminal?

A

V-G sodium
V-G potassium
V-G calcium

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2
Q

What is the difference between intracellular and extracellular calcium concentration?

A

10,000 fold

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3
Q

Describe the structure of a V-G calcium channel.

A

Very similar to V-G sodium channels
Four repeats each consisting of 6 transmembrane domains
Porphyrin alpha subunit
Only one needed for channel formation

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4
Q

What type of blockers act on L-type V-G calcium channels?

A

Dihydropyridines

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5
Q

Describe the subunit composition of calcium channels.

A

Porphyrin alpha subunit associated w/other subunits which fine tune properties and allow correct regulation of activity

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6
Q

How does calcium influx cause transmitter release?

A

Calcium influx –> binds to synaptotagmin –> brings vesicles close to plasma membrane –> snare complex makes fusion pore –> transmitter released through pore

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7
Q

What is synaptotagmin?

A

A protein which brings vesicles close to plasma membrane

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8
Q

How does increasing intracellular calcium affect transmitter release?

A

Increases

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9
Q

What affect does an increase in the number of action potentials to the nerve terminal have?

A

Increases pulses of transmitter released

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10
Q

How many subunits does a V-G calcium channel have?

A

5; incl. 2 alpha subunits

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11
Q

Where are nicotinic AChR found?

A

NMJ

Fast synaptic receptors

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12
Q

What feature of nAChR allows them to be used in fast synaptic receptors?

A

They allows fast depolarisation

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13
Q

How is an nAChR activated?

A

2 ACh molecules bind causing a conformational change that opens channels

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14
Q

What does the nACHR in an NMJ try to achieve with the membrane potential?

A

To reach -10 mV therefore causing depolarisation of the skeletal muscle fibre

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15
Q

How selective is the sodium-potassium channel?

A

Not very - equally permeable to both so ion movement is determined by equilibrium potential

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16
Q

What happens to the sodium-potassium channel at a membrane potential of -10 mV?

A

Reversal voltage is met
No net flow of charge
Current through channel reverses

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17
Q

What causes the end-plate potential?

A

ACh action on nAChR

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18
Q

How does decreasing extracellular calcium affect the end-plate potential?

A

Decreases amplitude

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19
Q

What are the sequence of events during neuromuscular transmission?

A

AP in neurone –> ACh release –> activate nAChR –> brief depolarisation (end-plate potential) –> adjacent sodium channels activated by local spread of charge –> excitation-contraction coupling

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20
Q

What are the two types of nAChR blockers?

A

Competitive

Depolarising

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21
Q

What is the mechanism of activation of tubocurarine?

A

Competitive blocker
Binds to alpha subunit but does not cause a conformational change
Decreases depolarisation without changing ACh amount

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22
Q

Can competitive nAChR blockers be overcome?

A

Yes - vastly increase ACh concentration

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23
Q

Which enzyme breaks down succinylcholine?

A

Plasma cholinesterase

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24
Q

Can depolarising nAChR blockers be overcome?

A

Nope

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25
Q

Describe the action of depolarising nAChR blockers.

A

Binds to alpha subunit –> receptor opens –> no AChE caused degradation –> receptor remains open –> sustained depolarisation –> sodium channels inactivated and receptors desensitised

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26
Q

What causes miniature end-plate potentials?

A

Spontaneous release of ACh vesicles w/out AP stimulus

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27
Q

What is the rate of ACh release in a miniature end-plate potential?

A

~1 quanta per second

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28
Q

What is the significance of the miniature end-plate potential?

A

It can be recorded (but does not reach anywhere near threshold potential)

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29
Q

What is myasthenia gravis?

A

Autoimmune targeting of nAChR

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30
Q

How are functional nAChR lost in myasthenia gravis?

A

Complement mediated lysis

Receptor degradation

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31
Q

What measurement can be used to determine myasthenia gravis and what does it show?

A

End-plate potentials - each quanta released gives a decreased response in comparison to unaffected muscle

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32
Q

S/S of myasthenia gravis?

A

Profound weakness
Muscle weakness increases w/exercise
Muscle fatigue

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33
Q

Where are muscarinic AChR found?

A

NMJ of parasympathetic branch of the ANS

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34
Q

Which give a faster response, nAChR or mAChR?

A

nAChR

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35
Q

Summarise the activation of an mAChR in one sentence.

A

ACh binds to the receptor causing the associated G-protein to split, allowing the alpha G-protein subunit to modify the activity of the target effector

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36
Q

Do both nAChR and mAChR use ligand binding?

A

Yes

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37
Q

Why are mAChR slower to initiate a response than nAChR?

A

They are coupled to G-proteins which trigger a cascade of events in the cell to cause a response. They do not have an ion channel like nAChR

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38
Q

What is calcium responsible for?

A

Bone and teeth integrity, fertilisation, proliferation, secretion, neurotransmission, metabolism, contraction, learning, memory, apoptosis, neurons etc.

39
Q

What is the advantage of having a large inward calcium gradient?

A

Changes in calcium are rapid w/small amounts of calcium ion movement

40
Q

What are the disadvantages of having a large inward calcium gradient?

A

Calcium overload is easy

Rapid loss of calcium regulation can lead to cell death

41
Q

How is the calcium gradient set-up and maintained?

A

Relative impermeability of the plasma membrane
Cell ability to expel calcium
Calcium buffers
Intracellular calcium buffers

42
Q

Which two transporter mechanisms are used to expel calcium across the CSM?

A

Calcium-ATPase

Sodium/calcium exchanger

43
Q

What is calmodulin?

A

A high affinity, low capacity trigger protein used for calcium expulsion

44
Q

Name three calcium binding proteins.

A

Synaptotagmin
Calmodulin
Troponin

45
Q

What factors of calcium binding molecules affect the diffusion of calcium?

A

Concentration

Saturation

46
Q

What two types of intracellular calcium stores are there?

A

Rapidly and non-rapidly releasable stores

47
Q

Where are rapidly releasable intracellular calcium stores found?

A

Sarcoplasmic reticulum

Endoplasmic reticulum

48
Q

What pump is used to release calcium from rapidly releasable stores?

A

SERCA

49
Q

What does SERCA require?

A

A low affinity, high capacity binding protein - e.g. Calsequestrin

50
Q

Where are non-rapidly releasing calcium stored found?

A

Mitachondria

51
Q

How does the calcium gradient across a mitochondria membrane compare to that across the cell membrane?

A

It is much greater

52
Q

When will mitochondria take up calcium?

A

When the intracellular concentration is high

53
Q

Why does mitochondrial uptake of calcium have to match energy demand and supply?

A

It requires ATPases

54
Q

Describe the mechanism of uptake of calcium by mitochondria.

A

Uniporter uses driving force from respiratory chain hydrogen ion production

55
Q

What are the properties of the uni porter used for calcium uptake in the mitochondria?

A

Low affinity

High capacity

56
Q

How is the internal calcium concentration elevated and returned to basal levels?

A

Calcium influx across the plasma membrane
Calcium release from rapidly releasable intracellular stores
Calcium release from non-rapidly releasable intracellular stores

57
Q

Which two channels are involved in influx of calcium across the plasma membrane?

A

V-G calcium channels

Receptor-operated calcium channels

58
Q

Give some examples of receptors used for receptor-operated calcium channels.

A

NMDA
AMPA
Glutamate receptors (especially in the brain)
Some nAChR

59
Q

What is the term given to describe receptor-operated calcium channels?

A

Inotropic channels

60
Q

How do V-G calcium channels operate?

A

Depolarisation –> conformational change

61
Q

How do receptor-operated calcium channels work?

A

Ligand/agonist binds –> opens aqueous pore –> calcium can move in

62
Q

Why will mitochondria take up calcium?

A

They need a high concentration to stimulate mitochondrial metabolism

63
Q

What is the role of mitochondria in calcium regulation?

A 
Buffering
Signalling
Match energy demand and supply
Apoptosis
Altered redox potential
64
Q

By which two methods is the release of calcium from rapidly releasable intracellular stores mediated?

A

G-protein coupled receptors

Calcium-induced calcium release

65
Q

Describe the mechanism of GPCRs in calcium release from non-rapid stores.

A

Ligand/agonist binds to GPCR –> turns receptor on –> effector molecules activated –> cellular response

66
Q

Which two effector molecules are stimulated by activation of GPCRs?

A

Plasma channels

Muscarinic receptors

67
Q

How can the activation of GPCRs lead to different cellular responses in different cells?

A

Different muscarinic receptors are present in different cells - M1 to M5

68
Q

What is the function of alpha-q once it has split from the 7-transmembrane domain of the GPCR?

A

It activates phospholipase C which activates IP3 and diacylglycerol

69
Q

What is the action of IP3?

A

Ligand-gated ion channels found in the sarcoplasmic/endoplasmic reticulum which have a pore permeable to calcium, allowing its efflux from the S/ER to increase cellular calcium levels

70
Q

What is the action of diacylglycerol?

A

Protein kinase C regulation

71
Q

What molecule do alpha-s and alpha-I have opposite actions on?

A

Adenyl cyclase

72
Q

What is the mechanism of adenylyl cyclase action?

A

Produces cAMP –> phosphorylates protein kinase A

73
Q

Where are M3 receptors found?

A

Walls of the airways

74
Q

What does activation of the M3 receptors cause?

A

Contraction of smooth muscle in the airways

75
Q

Where is ryanodine derived from?

A

Plants

76
Q

Where are ryanodine receptors found?

A

In the sarcoplasmic/endoplasmic reticulum

77
Q

How are ryanodine receptors activated?

A

Conformational coupling with voltage operated calcium channels
Depolarisation

78
Q

How does calcium exit through ryanodine receptors?

A

Acts as an agonist –> conformational change –> released

79
Q

How does depolarisation of the T-tubule cause calcium release?

A

V-G sodium channels open

VOCC open

80
Q

Why are the ryanodine receptors so important for calcium release?

A

Give explosive release of 85% of calcium

Located directly adjacent to contractile proteins

81
Q

What happens in the cardiac myocyte when calcium levels decrease?

A

Ryanodine receptor stops
SERCA pumps calcium into stores
NCX reverses –> calcium into T-tubule for minor store

82
Q

What restores normal function of the NCX following decreased calcium levels?

A

Sodium removal

83
Q

What causes the plateau in the cardiac action potential before repolarisation occurs?

A

Calcium influx via VOCC

84
Q

What is the role of calcium in muscle contraction?

A

Bind with tropomyosin and roll it out of the way

Exposes binding sites for cross-bridge recycling

85
Q

How are microdomains formed?

A

Strategically placed calcium channels allow local variations in calcium levels

86
Q

Why does repetitive signalling need restoration of basal calcium levels?

A

Too much calcium for too long is toxic

87
Q

How do cells return intracellular calcium concentrations to basal levels?

A

Use of transient signals

88
Q

What does return of calcium to basal levels require?

A

Termination of signal
Calcium ion removal
Calcium ion store refilling

89
Q

How are calcium stores refilled?

A

Recycling of released cytosolic calcium
VOCC
Capacitative/store operated calcium channel

90
Q

Describe the mechanism of recycling released calcium.

A

In cardiac myocytes effectively release and grab back cytosolic calcium

91
Q

Describe the mechanism of channel led calcium store refilling.

A

Deleted signal to membrane allows more calcium in

Specific proteins interact to activate the channel

92
Q

What is STIM-ER?

A

ER membrane located calcium sensor w/motif that binds to calcium which causes a conformational change

93
Q

What is ORAI?

A

A plasma membrane channel which allows entry of calcium

94
Q

Can channel led calcium store refilling regulate physiological processes?

A

Yes

95
Q

Is the mechanism of calcium regulation always the same?

A

No, it may be dependent on cell type and circumstance

Semester 2 (45 decks)

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