Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Which channels are found in the nerve terminal?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between intracellular and extracellular calcium concentration?

A

10,000 fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Dihydropyridines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is synaptotagmin?

A

A protein which brings vesicles close to plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does increasing intracellular calcium affect transmitter release?

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Increases pulses of transmitter released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

5; incl. 2 alpha subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are nicotinic AChR found?

A

NMJ

Fast synaptic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

They allows fast depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is an nAChR activated?

A

2 ACh molecules bind causing a conformational change that opens channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How selective is the sodium-potassium channel?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes the end-plate potential?

A

ACh action on nAChR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Decreases amplitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two types of nAChR blockers?

A

Competitive

Depolarising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Can competitive nAChR blockers be overcome?

A

Yes - vastly increase ACh concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which enzyme breaks down succinylcholine?

A

Plasma cholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Can depolarising nAChR blockers be overcome?
Nope
25
Describe the action of depolarising nAChR blockers.
Binds to alpha subunit --> receptor opens --> no AChE caused degradation --> receptor remains open --> sustained depolarisation --> sodium channels inactivated and receptors desensitised
26
What causes miniature end-plate potentials?
Spontaneous release of ACh vesicles w/out AP stimulus
27
What is the rate of ACh release in a miniature end-plate potential?
~1 quanta per second
28
What is the significance of the miniature end-plate potential?
It can be recorded (but does not reach anywhere near threshold potential)
29
What is myasthenia gravis?
Autoimmune targeting of nAChR
30
How are functional nAChR lost in myasthenia gravis?
Complement mediated lysis | Receptor degradation
31
What measurement can be used to determine myasthenia gravis and what does it show?
End-plate potentials - each quanta released gives a decreased response in comparison to unaffected muscle
32
S/S of myasthenia gravis?
Profound weakness Muscle weakness increases w/exercise Muscle fatigue
33
Where are muscarinic AChR found?
NMJ of parasympathetic branch of the ANS
34
Which give a faster response, nAChR or mAChR?
nAChR
35
Summarise the activation of an mAChR in one sentence.
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
36
Do both nAChR and mAChR use ligand binding?
Yes
37
Why are mAChR slower to initiate a response than nAChR?
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
38
What is calcium responsible for?
Bone and teeth integrity, fertilisation, proliferation, secretion, neurotransmission, metabolism, contraction, learning, memory, apoptosis, neurons etc.
39
What is the advantage of having a large inward calcium gradient?
Changes in calcium are rapid w/small amounts of calcium ion movement
40
What are the disadvantages of having a large inward calcium gradient?
Calcium overload is easy | Rapid loss of calcium regulation can lead to cell death
41
How is the calcium gradient set-up and maintained?
Relative impermeability of the plasma membrane Cell ability to expel calcium Calcium buffers Intracellular calcium buffers
42
Which two transporter mechanisms are used to expel calcium across the CSM?
Calcium-ATPase | Sodium/calcium exchanger
43
What is calmodulin?
A high affinity, low capacity trigger protein used for calcium expulsion
44
Name three calcium binding proteins.
Synaptotagmin Calmodulin Troponin
45
What factors of calcium binding molecules affect the diffusion of calcium?
Concentration | Saturation
46
What two types of intracellular calcium stores are there?
Rapidly and non-rapidly releasable stores
47
Where are rapidly releasable intracellular calcium stores found?
Sarcoplasmic reticulum | Endoplasmic reticulum
48
What pump is used to release calcium from rapidly releasable stores?
SERCA
49
What does SERCA require?
A low affinity, high capacity binding protein - e.g. Calsequestrin
50
Where are non-rapidly releasing calcium stored found?
Mitachondria
51
How does the calcium gradient across a mitochondria membrane compare to that across the cell membrane?
It is much greater
52
When will mitochondria take up calcium?
When the intracellular concentration is high
53
Why does mitochondrial uptake of calcium have to match energy demand and supply?
It requires ATPases
54
Describe the mechanism of uptake of calcium by mitochondria.
Uniporter uses driving force from respiratory chain hydrogen ion production
55
What are the properties of the uni porter used for calcium uptake in the mitochondria?
Low affinity | High capacity
56
How is the internal calcium concentration elevated and returned to basal levels?
Calcium influx across the plasma membrane Calcium release from rapidly releasable intracellular stores Calcium release from non-rapidly releasable intracellular stores
57
Which two channels are involved in influx of calcium across the plasma membrane?
V-G calcium channels | Receptor-operated calcium channels
58
Give some examples of receptors used for receptor-operated calcium channels.
NMDA AMPA Glutamate receptors (especially in the brain) Some nAChR
59
What is the term given to describe receptor-operated calcium channels?
Inotropic channels
60
How do V-G calcium channels operate?
Depolarisation --> conformational change
61
How do receptor-operated calcium channels work?
Ligand/agonist binds --> opens aqueous pore --> calcium can move in
62
Why will mitochondria take up calcium?
They need a high concentration to stimulate mitochondrial metabolism
63
What is the role of mitochondria in calcium regulation?
``` Buffering Signalling Match energy demand and supply Apoptosis Altered redox potential ```
64
By which two methods is the release of calcium from rapidly releasable intracellular stores mediated?
G-protein coupled receptors | Calcium-induced calcium release
65
Describe the mechanism of GPCRs in calcium release from non-rapid stores.
Ligand/agonist binds to GPCR --> turns receptor on --> effector molecules activated --> cellular response
66
Which two effector molecules are stimulated by activation of GPCRs?
Plasma channels | Muscarinic receptors
67
How can the activation of GPCRs lead to different cellular responses in different cells?
Different muscarinic receptors are present in different cells - M1 to M5
68
What is the function of alpha-q once it has split from the 7-transmembrane domain of the GPCR?
It activates phospholipase C which activates IP3 and diacylglycerol
69
What is the action of IP3?
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
What is the action of diacylglycerol?
Protein kinase C regulation
71
What molecule do alpha-s and alpha-I have opposite actions on?
Adenyl cyclase
72
What is the mechanism of adenylyl cyclase action?
Produces cAMP --> phosphorylates protein kinase A
73
Where are M3 receptors found?
Walls of the airways
74
What does activation of the M3 receptors cause?
Contraction of smooth muscle in the airways
75
Where is ryanodine derived from?
Plants
76
Where are ryanodine receptors found?
In the sarcoplasmic/endoplasmic reticulum
77
How are ryanodine receptors activated?
Conformational coupling with voltage operated calcium channels Depolarisation
78
How does calcium exit through ryanodine receptors?
Acts as an agonist --> conformational change --> released
79
How does depolarisation of the T-tubule cause calcium release?
V-G sodium channels open | VOCC open
80
Why are the ryanodine receptors so important for calcium release?
Give explosive release of 85% of calcium | Located directly adjacent to contractile proteins
81
What happens in the cardiac myocyte when calcium levels decrease?
Ryanodine receptor stops SERCA pumps calcium into stores NCX reverses --> calcium into T-tubule for minor store
82
What restores normal function of the NCX following decreased calcium levels?
Sodium removal
83
What causes the plateau in the cardiac action potential before repolarisation occurs?
Calcium influx via VOCC
84
What is the role of calcium in muscle contraction?
Bind with tropomyosin and roll it out of the way | Exposes binding sites for cross-bridge recycling
85
How are microdomains formed?
Strategically placed calcium channels allow local variations in calcium levels
86
Why does repetitive signalling need restoration of basal calcium levels?
Too much calcium for too long is toxic
87
How do cells return intracellular calcium concentrations to basal levels?
Use of transient signals
88
What does return of calcium to basal levels require?
Termination of signal Calcium ion removal Calcium ion store refilling
89
How are calcium stores refilled?
Recycling of released cytosolic calcium VOCC Capacitative/store operated calcium channel
90
Describe the mechanism of recycling released calcium.
In cardiac myocytes effectively release and grab back cytosolic calcium
91
Describe the mechanism of channel led calcium store refilling.
Deleted signal to membrane allows more calcium in | Specific proteins interact to activate the channel
92
What is STIM-ER?
ER membrane located calcium sensor w/motif that binds to calcium which causes a conformational change
93
What is ORAI?
A plasma membrane channel which allows entry of calcium
94
Can channel led calcium store refilling regulate physiological processes?
Yes
95
Is the mechanism of calcium regulation always the same?
No, it may be dependent on cell type and circumstance

Semester 2 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions