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biomembranes > KV channels > Flashcards

KV channels Flashcards

1
Q

how many KV channels are there in the human genome

A

over 70

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2
Q

what do KV channels contribute to

A

control of cell volume
control of membrane potential and cell excitability
secretion of salts, hormones and neurotransmitters

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3
Q

what can KV channels be regulated by

A

hormones and transmitters
voltage across membrane
conc of Ca2+ or ATP in cytoplasm
kinase and phosphatases
G-proteins

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4
Q

what do KV channels respond to

A

electrochemical gradient (missing the voltage sensor)

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5
Q

what are KV responsible for

A

shaping of the AP

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6
Q

in native cells, what are the 2 main types of KV

A

inactivating (‘A’) type
non-inactivating (delayed recifier)

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7
Q

inactivation of KV channels (ball and chain model)

A

‘A’ type K+ channels display rapid inactivation following opening - deletion of residued 6 to 46 caused currents which displayed no inactivation
inactivation caused by first 20 AAs - which forms compact hydrophobic/charged surfct domain (the ball) following 50-60 AA form the ‘chain’

basically when a cell is being stimulated, ball/chain loops and blocks channel which inactivates it

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8
Q

what is ion selectivity of K channels determined by

A

carbonyl backbone groups of the TVGYG motif in the P loop

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9
Q

what is the ball and chain model often reffered to as

A

N-type inactivation (involved N-terminus structure)

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10
Q

what constitues the receptor for the inactivation ball

A

a set of AAs in the S4-S5 loop (near the internal channel mouth)

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11
Q

what can addition of b-subunits do

A

induce fast inactivation

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12
Q

what is the function of calcium-activated K+ channels modulated by

A

Ca2+

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13
Q

what are the sybtypes of calcium-activated K+ channels

A

large conductance (~250pS) K+ channels (aka BK)
KCa or Maxi-K channels
intermediate conductance channels (IK - 60-100pS)
small conductance channels (SK - </=20pS)

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14
Q

in neurons, what are SK channeks responsible for

A

slow afterhyperpolarisation (AHP) observed after AP discharges

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15
Q

where are maxi-K channels expressed

A

ubiquitously except the heart

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16
Q

what do maxi-K channels do within neurons

A

help shape APs and regulate transmitter release

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17
Q

what do maxi-K channels do in smooth muscle

A

help regulate contractility and tone

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18
Q

how are maxi-K channels opened

A

they are voltage-dependant - so opening is controlled by transmembrane voltage (gated by depolarisation)

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19
Q

what is the activation voltage of K+ channels dependant on

A

intracellular CA2+ concentratoon
as the Ca2+ conc increases, the channel required less electrical energy to open

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20
Q

describe the structure of the maxi-K channnel

A

extra transmembrane domain at N-terminal region, resulting in exoplasmic NH2 terminus
long COOH terminus region

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21
Q

what encodes a Maxi-K a subunit

A

a single gene (slo)

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22
Q

what happens when b1-b4 interact with Maxi-K subunit

A

alter Ca2+ sensitivity and voltage, activation kinetics and pharmacology

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23
Q

what is required for he b subunit modulation of channels

A

S0/N-terminal domain

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24
Q

what does the a subuniy primary sequence contain

A

possible phosphorylation sites and additions of splice insertions adds more - resulting in channels differentially regulated by protein kinases/phosphatases

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25
Q

where are Maxi-K channels abundant

A

mammalian CNS and smooth muscle

26
Q

what domains does maxi-k have

A

voltage-gated and ligand-gated

27
Q

what is the typical voltage sensor within the Kv channel

A

S4 region acting as voltage sensor (as maxi-K does not possess a voltage sensor)

28
Q

what does the ligand-gated mechanism involve

A

specialized structures present in the C-terminal region of the protein

29
Q

what do RCK (regulator of conductance of K+) domains contribute to

A

binding of an intracellular ligand

30
Q

where are hydrophobic segments found

A

in the C-terminus

31
Q

what does pressure on the RCK lead do

A

a conformational change (when Ca2+ is bound)

32
Q

what determines the Ca2+ sensitivity of the channel

A

tail domain of alpha subunit - region between S9 and S10 - contains a series of negatively charged (D) residues

33
Q

what happens when there is mutations in the region between S9 and S10

A

effect high affinity sensing of calcium

34
Q

what does increasing intracellular calcium lead to

A

increases the opening force on the channel gates (bc it has bound to these sites) - which leads to increased channel opening

35
Q

why is the maxi-K an important feedback system for calcium entry in many cell types

A

because of its sensitivity to calcium

36
Q

what does maxi-K play an important role in

A

timing of bursts of APs - also contributes to AHP

37
Q

maxi-K role in vascular reactivity

A

they induce hyperpolarization and balance the effects of excessive vasoconstriction - open in response to local elevations of Ca2+ and relax smooth muscle (close Ca2+ channels)

38
Q

what correlates to hypertension

A

loss of B1 subunit
(no B1 subunit - maxi-K is less Ca2+ sensitive, and so get increased arterial tone and BP)

39
Q

how do maxi-K channels provide a mechanism for cochlear hair frequency tuning

A

various splice varients of a subunit, in combination with b subunits and CaV channels - determines frequency to which each hair cell responds - frequency encoding in hearing

40
Q

how to maxi-K channels contribute to vascular smooth muscle relaxation

A

Ca release by CICR via ryanodine receptors causes local increase in [Ca]i, this activates BK channels which gives K efflux, which hyperpolarizes the membrane which closes CaV that gave the initial depolarization and contraction - and so the smooth muscle relaxes

41
Q

where are maxi-K channels present at high levels

A

axon terminals, somas and dendrites

42
Q

what happens when you block maxi-K channels

A

AP is broadened, AHP is diminished

43
Q

how many loops are required to make a functional K+ channel

A

4

44
Q

what does ratification mean

A

structural elements in channel which ensure movement of channel in only one direction

45
Q

explain the two TM domain

A

one pore family consist of the inward rectifiers - these channels conducy K+ currents more in the inward direction than the outward and help set RMP

46
Q

explain the four TM domain

A

two pore family are weak inward rectifiers - most abundant class of K+ channels - act as ‘background’ channels and help set RMP

47
Q

what are TREK1 channels

A

signal integrators

48
Q

what do TREK1 channels respond to

A

many inputs of mechanical deformation
- internal pH reduction
- heat
- intracellular lipids
- fatty acids

49
Q

what happens when TREK1 channels are activated

A

increased channel opening and hyperpolarization of RMP

50
Q

how does inhibition of TREK1 occur

A

phosphorylation of intracellular sites via PKC and PKA

51
Q

what can open TREK1

A

various votile and gaseous anaesthetic agents

52
Q

where is human TREK1 highly expressed

A

in the brain

53
Q

functions of TREK1 (as seen in mice)

A
  • decreased sensitivity to anaesthetics
  • more sensitive to brain ischemia and epilepsy
  • loss of neuroprotection from polyunsaturated fatty acids
  • mood regulation (anti-depressant)
54
Q

what happens when TREK1 opens in presynaptic terminals

A

closes CaV channels and decreases release of neurotoxic glutamate

55
Q

what hppens when TREK1 opens in postsynaptic sites

A

hyperpolarising of the cell and increased NMDA receptor Mg2+ block - reduced excitotoxicity

56
Q

give examples of potassium channel openers (KCOs)

A

cromakalim
pinacidil
minoxidil
diazoxide

57
Q

what is diazoxide occasionally used to do

A

decrease insulin secretion from beta cells

58
Q

KCOs relax

A

smooth muscle

59
Q

when GTP is bound to G proteins…

A

K+ channels open

60
Q

what is the activity of G-protein terminated by

A

intrinsic GTPase activity of the G-protein itself - converting GTP to GDP

biomembranes (9 decks)

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