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Year 1 > Voltage gated ion channels & GPCRs > Flashcards

Voltage gated ion channels & GPCRs Flashcards

1
Q

A voltage gated channel has ___ TMD, ___ subunits, and a total of ___ TMDs

A

6 TMDs, 4 subunits, total of 24 TMDs

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2
Q

voltage sensor

A

S4

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3
Q

Different pieces of the N terminal are involved in these 2 events

A
  1. targeting and assembly of information

2. inactivation region to turn channel off

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4
Q

What does the alpha subunit consist of? (2)

A

Voltage sensor (S4), and Pore region (P)

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5
Q

What is the importance of the beta subunit? (4)

A

need beta’s:

  1. to get full inactivation
  2. timing
  3. correct V-response
  4. during biosynthesis, need as chaperone from ER to surface
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6
Q

Order of ion selectivity from least to greatest:

A

gap junction (large pore formed by connexins) < ligand-gated channels (middle size pore) < voltage gated channels < pumps

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7
Q

What is the basic structure of the voltage sensor? How does it become reactive?

A

Made up of arginines and lysines, one cysteine that is unreactive, but when cell depolarizes, the sensor moves closer to outside to cell. Reagants can react with cysteine.

recall cysteine can form disulfide bonds; will react with sulfhydryl reagents (membrane-impermeant tags)

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8
Q

What part of the voltage gated channel contains the ion selectivity? (ion selectivity is doing the conductance)

A

The pore loop (can plug in different pore loops to get different channels)

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9
Q

Two types of K+ channels:

A
  1. one that turns on and stays on
  2. one that turns on and turns right back off
    > you need #2 for auditory reasons, otherwise you would only hear low rumbles. to hear higher frequencies, auditory nerve needs to follow vibrations for sound one for one.
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10
Q

autosomal recessive disorder, experiences no pain

A

CIP = channelopathy-associated insensitivity

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11
Q

autosomal dominant disorder characterized by burning pain in the rectal, ocular, and mandibular areas

A

PEPD = paroxysmal extreme pain disorder

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12
Q

2 main types of effects of altered/mutant ion channels

A
  1. slow channel inactivation

2. shift threshold voltage for g(na+), either up toward 0 or down closer to resting potential

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13
Q

PEPD and CIP mutation found in

A

SCN9A, also called Nav1.7

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14
Q

What is SCN?

A

They are all sodium channels (hence S), alpha-subunit of the voltage gated sodium channel

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15
Q

In paroxysmal extreme pain disorder, what type of channel is it?

A

Hyperfunctioning (autosomal dominant, because if conveying pain, one is enough to feel pain)

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16
Q

In channelopathy-associated insensitivity to pain, what type of channel is it?

A

Nonexistent channel (autosomal recessive because 1 okay copy is enough to be normal)

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17
Q

6 TMDs form homo or hetero-____. Two examples

A

tetramers. Potassium and Transient receptor potential channel (TRP= looks like potassium, big family, over 30, sense pH)

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18
Q

4 TMDs form ____. One example

A

hexamers; connexins (gap junctions)

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19
Q

2 TMDs form ____

A

tetramers, with associated beta chains (net 6 TMD per subunit), has friends so still can make 24

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20
Q

ATPase pumps (2)

A
  1. Na+/K+ pump

2. Ca2+ pump (H+ in, Ca2+ out)

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21
Q

Ion exchangers (2) “gradient riders”

A
  1. Na+/Ca2+ (Na in/down conc gradient, Ca out)

2. Na+/H+ (Na in, H out)

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22
Q

Co-transporters (3) “gradient riders”

A
  1. Na+/K+/Cl- (all in)
  2. K+/Cl- (K out, Cl out)
  3. Na+/neurotransmitter, GABA, DA (both in)
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23
Q

This drug meses up the V-ATPase pump, developed during WIII, has huge side effect problems

A

Chloroquine

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24
Q 
Important molecular properties of Na+/K+ pump
describe binding locations of following:
1. ouabain (poison)
2. Na and K 
3. location of alpha and beta subunits
3. Phosphorylation and ATP
A
  1. ouabain binding site is outside cell
  2. Na and K binding is is transmembrane sites
  3. N terminals are alpha and beta subunits inside cell
  4. Phosphorylation and ATP binding site are on loops inside the cell
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25
Q

In mature neuron, this channel transports K out with Cl-, so when GABA and Gly open anion channels, Cl enters cell, and get inhibitory effect

A

KCC2, KCC3

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26
Q

In immature neuron, this channel brings Na, K, and 2 Cl all into cell. When channel opens and GABA/Gly bond, Cl-leaves cell, and get excitatory effect

A

NKCC1

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27
Q

If looking at sodium efflux from cells, what would cause a huge drop in its efflux rate?

A

Drop would occur if you take away potassium. as soon as you put back in, it goes back to normal. Same happens if you block ATP synthesis

= energy dependent pump that requires K on outside to get sodium from inside to out

28
Q

How many TMDs does a GPCR have?

A

7 TMDs

29
Q

In the GPCR structure, the N terminal is located in the (cytosol/outside), while the C-terminal is located in the (cytosol/outside).

A 
N-terminal = outside
C-terminal = cytosol
30
Q

in the alpha beta gamma complex known as the “heterotrimeric G protein,” alpha subunit binds what nucleotide?

A

guanine nucleotide

31
Q

The alpha subunit is inactivated by _____ and internalized bound to ______

A

GRK = G protein receptor kinase

arrestin

32
Q

What does the beta gamma complex affect?

A

ion channels

33
Q

in amplification in the second messenger cascade, one ligand binding event results in how many cAMP?

A

100 cAMP molecules form one ligand binding event

34
Q

each cAMP activated how many protein kinase A (PKAs)?

A

1 molecules of PKA

35
Q

each PKA phosphorylates how many proteins?

A

100 proteins, which in turn could affect more molecules

36
Q

How many GRK genes? How many arrestin genes?

A

7 GRK, 4 arrestin

37
Q

In GPCR, 1 ligand binding produces how many phosphoproteins?

A

10,000

38
Q

Differences in receptor for GPCR vs. ligand gated channels

A

ligand gated ion channel- receptor is source of measured response, the conductance change

GPCR-several steps before end biological response is seen

39
Q

In addition to difference in receptor action, what is the other major difference between GPCR and ligand gated ion channels?

A

GPCR can act singly or as dimers, but not in higher order conglomerates typical of ligand gated ion channels

40
Q

There are over 1000 GPCRS in human genome, yet half are “orphan receptors.” What does this mean?

A

They have no known ligand yet

41
Q

There are many genes for each alpha, beta, and gamma in the GPCR complex. How many receptor genes are there usually for any one ligand?

A

typically about 6.

42
Q

What is the alpha subunit most crucial for?

A

The sign or direction of the response (alpha-s subunit - stimulating adenylate cyclase while alpha-i inhibits, etc)

43
Q

G protein Receptor Kinases (GRKs) come in these three classes:

A
  1. rhodopsin kinase (GRK1) and cone kinase (GRK7)- visual system only
  2. beta-adrenergic receptor kianses (GRK 2,3)
  3. GRKs 4, 5, 6
44
Q

Targets of phosphorylation and ubiquitinylation, and targets the receptors for internalization and recycling to the cell surface, or for degradation

A

Arrestin

45
Q

Why does the nervous system use GPCRs? (4)

A
  1. amplification
  2. timing (100 msec to seconds or minutes)
  3. spatial effects (signaling over larger physical range)
  4. integration (cross talk, “molecular memory”
46
Q

In general, mechanical senses like touch, somatosensory, and hearing use what type of channels?

A

Ion channels

47
Q

Potential explanation for why vision uses GPCR

A

need for massive amplification to get optimal sensitivity to low light, yet adapt to very bright light

48
Q

What type of channel does taste use?

A

GPCR and ion channels, tastants come in ionized and lipid-soluble forms

(salts and acids-ion channels. sweets-GPCRs).

49
Q

This nonspecific cation channel is activated in vision

A

CNGC (Cyclic Nucleotide Gated Channel)

50
Q

What activated CNGC?

A

cAMP

51
Q

In the retina, where does the light reception occur?

A

At the discs within the outer segments of the rods

52
Q

The name of the GPCR for light

A

opsin

53
Q

This opsin (GPCR for light) is for rods, which detect black and white low lighting conditions

A

Rhodopsin

54
Q

The G protein owned by visual system

A

transducin

55
Q

The signal from light travels from the disc membrane through transducin to activate this enzyme

A

phosphodiesterase

56
Q

Once activated, what does phosphodiesterase do?

A

Chews up cGMP (which was high and activating GNFC, which is “on” or open in the dark)

57
Q

What happen once CNGC shuts down and closes?

A

The rod (or cone) hyperpolarizes (because CNGC=non specific cation channel, so blocking a lot of cations from entering cell) and slows down neurotransmitter release to cells downstream

58
Q

How many photons are absorbed by 1 rhodopsin?

A

1 photon

59
Q

1 rhodopsin activates how many transducins?

A

hundreds of transducins

60
Q

How many phosphodiesterses are activated by one transducin?

A

1:1 activation of phosphodiesterase

61
Q

How many cGMPs get hydrolyzed/”chewed up” by one phosphodiesterase?

A

100,000 cGMPS

62
Q

hundreds of Na+ channels close in response to phosphodiesterase chewing up cGMPs (which are responsible for activating CNGC, which is “on” or open in the dark). How many Na+ ions are thus denied entry as a result?

A

1-10,000,000 ions

63
Q

as a result of closed Na+ channels, how much is the rod membrane hyperpolarized?

A

1 mV-detectable in perception

64
Q

GPCRs can activate/inhibit these two important enzymes

A

adenylate cyclase, and phospholipase C

65
Q

Phospholipase C can cleave what in the membrane and what in the cytosol?

A

Cleave PIP2 to diacylglycerol (DAG) in membrane

cleaves IP3 in cytosol

66
Q

Explain why kinases are described as intrinsically active with a built in “muzzle”

A

Kinases all seem to have a negative regulatory domain. Turning off that silencing domain is key to activating the kinase.

Year 1 (48 decks)

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