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3922 > 6 - VGIC > Flashcards

6 - VGIC Flashcards

1
Q

The a subunit of VGICs can function on their own

A

True

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2
Q

What is the role of the b subunits of VGIC

A

Modulate the function of the alpha subunits

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3
Q

What are some of the actions of the b subunit (2)

A

Regulate expression levels, location and trafficking

Alter voltage dependence of activation or inactivation

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4
Q

What can bind to the b subunit

A

Drugs to module function

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5
Q

What does phosphorylation of the b subunit do

A

Regulate VGIC function

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6
Q

What controls the selectivity of VGICs for Na/K/Ca

A

Aqueous pore

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7
Q

How do VGICs open

A

Contain a voltage sensor which moves in response to changes in membrane potential

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8
Q

Regulatory domains in related channels can regulate opening of channels true or false

A

True, Ca activated K channels

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9
Q

What is deactivation

A

When the membrane potential reverses back to its resting state the channel may close

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10
Q

What is inactivation

A

Voltage dependent Na channels will close immediately after being activated even when there is still depolarisation

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11
Q

What is the Ball and Chain model for inactivation

A

Influx of +ve charge will cause an intracellular domain to swing into the open pore of the channel to prevent ion flow

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12
Q

What does phosphorylation of VGICs do

A

Alter channel properties such that it responds in a different manner to allow the cell to respond to different physiological stimuli - allows for rapid changes in channel function

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13
Q

What are two examples of phosphorylation of VGICs

A

1) Protein Kinase c causes phosphorylation of a single residue in the a subunit of a Nav to slow the rate of channel inactivation
2) Phosphorylation by Protein Kinase A slows the rate of Cav channel activation and shifts voltage depndence so that it is activated at more negative potentials

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14
Q

What are 3 parts of Nav(1.2)

A

Pore region
Voltage sensors
Linker between voltage sensor and pore

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15
Q

What would result from blocking all Nav channels

A

Complete loss of sensory system
Sedations
Coma

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16
Q

How do many Nav blocking drugs gain access to the channel

A

Binding to the open state of the pore i.e. only active neurones

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17
Q

How many main types of Na+ channel a subunits are there

A

9

18
Q

What do tetrodotoxins do

A

Bind to the external surface of the a subunit of the channel in the S5-S6 loop region and block the pore

19
Q

What are two drugs that modulate Nav activity

A

Phenytoin and carbamazepine

20
Q

What are phenytoin and carbamazepine used for

A

Treatment of epilepsy

Prevents seizure

21
Q

How do phenytoin and carbamazepine work

A

Slow the recovery from the inactivated state

Limits the firing rates of neurones

22
Q

What are 3 LAs

A

Cocaine
Lidocaine
Procaine

23
Q

How do LAs work

A

Bind to the Na+ channel at sites exposed to the lipid membrane to block the channel
Causes Na+ to bind to the inactivated state of the channel creating a use dependent blocke

24
Q

What do Kv channels do (3)

A

1) Set the cells resting membrane potential
2) Repolarise the cell after an action potential
3) Controlling the cell’s rate of firing and shape of the action potential

25
Q

What are the two types of K channels

A

6 TM K channels

2 TM K channels

26
Q

What do delayed rectifiers do

A

Delay activation after depolarisation and inactivate slowly - facilitate repolarisation

27
Q

What do A-type channels do

A

Transiently activate when a cell is depolarised after a period of hyperpolarisation - decreases firing frequency

28
Q

What do Ca-activated K channels so

A

Respond to Ca, remain open for prolonged period

Prolong hyperpolaisation

29
Q

What do inward rectifiers do

A

G-proteins that can regulate their activity (GIRKs)

30
Q

How does noradrenaline increase the firing activity of hippocampul pyramidal neurones

A

NA binds to B-adrenergic receptor which stimulates cAMP production and PKA activity
PKA phosphorylates Ca activated K channels and blocks their activity
Hyperpolarisation is reduced and neuron is kept in excitable state allowing more firing

31
Q

Are many K channel blockers used to treat neurological disorders

A

No despite a wide variety

32
Q

What is a useful K inhibitor research tool

A

Tetraethylamonium

33
Q

What inhibits delayed rectifiers

A

Cs

34
Q

What can Ca entry into cells trigger (6)

A

1) Muscle contraction
2) Neurotransmitter release
3) Activation of second messenger systems
4) Alteration in gene expression
5) Apoptosis
6) Depolarisation - Ca2+ spikes

35
Q

Where are L-type Ca channels found

A

Cell body

Proximal dendrite

36
Q

Where are Ca1.1 found

A

Skeletal muscle

37
Q

Where are Ca1.2 found

A

Cardiac muscle, smooth muscle, brain

38
Q

What do PQNR channels do

A

Regulate neurotransmitter release. Ca2+ influx through these channels causes release of NT

39
Q

What is a potential treatment for chronic pain

A

Synthetic peptide blocker of N-type channels

40
Q

What do T-channels mediate

A

Repetitive firing of neurones

41
Q

What is the MOA for Gabapentin and pregabalin

A

Bind to a2d subunit to disrupt trafficking of the channel to the membrane
Selective for CaV2.2 that regulate neurotransmitter release in sensory neurones

42
Q

What do cone snail toxins contain to modulate VGICs

A

Peptides to target ion channels, receptors and transporters involved in neurotransmission

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