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Biomembranes > Voltage Gated Ion channels > Flashcards

Voltage Gated Ion channels Flashcards

1
Q

what facet of a channel pore will determine the size of the pore and hence ion selectivity?

A
  • Amino acid residue side/diameter
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2
Q

Selectivity filter for K channels (think about the AA residues in Pore loop)?
hint: two components

A
  • carbonyl backbone groups of AAs
  • TVGYG in P loop
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3
Q

Selectivity filter for Na channels (think AA residues)?

A

-DEKA side chains

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4
Q

which transmembrane segment acts as the voltage sensor that detects depolarization, and what properties does it have?

A
  • segment 4
  • has Arg residues (positively charged)
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5
Q

what is the effect of a positive membrane potential on the S4 helical structure of a voltage gated ion channel?

A
  • positive residues of helix are repelled, leading to helix movement out of channel i.e. conformational change–> channel opening
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6
Q

what causes the preceding outward current during recording of Na ion movement during depolarization

A
  • outward movement of positive charges within S4
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7
Q

How are V-gated Na/Cl channels different from K channels (think about peptides needed to form channel)?

A
  • Na/Cl channels are formed from a single polypeptide
  • K channels formed from 4 polypeptides joined together
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8
Q

Describe the structure of the Alpha subunits voltage gated ion channels

A

each alpha subunit has 6 transmembrane regions consisting of a loop between TM5-TM6

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9
Q

significance for IFM (isoleucine, phenylalanine, Methionine) peptide motif in NaV channels?

A
  • hydrophobic triad that forms inactivation gate– acts as pore blocker
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10
Q

what is the result of having an Na channel:
- with (Wtype) IFM
- without (IFM–>QQQ mutation) IFM motif

A

IFM— keeps Na current brief during depolarization

IFM–>QQQ: no more inactivation– persisting Na cannel activation as long as there is stimulus

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11
Q

how long do NaV channels typically stay open for?
- what condition occurs after channel opens and repolarization begins?

A
  • 1 milisecond
  • channel opening is followed by closure/refractory period– no conductance
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12
Q

what single-current channel state is transiently favored by depolarization?

A
  • Open State
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13
Q

what single-current channel state is favored by hyperpolarization?

A
  • resting (closed) state
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14
Q

what single-current channel state is favored by maintained depolarization?

A
  • inactivated state
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15
Q

what is a consideration when thinking about P0 (probability of channel opening) value when calculating Whole cell current (I)

A
  • NOT all channels will be opend at x point in time
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16
Q

what kind of feedback loop drives Na entry upon activation Gate?

A
  • positive feedback loop
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17
Q

describe the relationship between Na current and magnitude of depolarization

A
  • amount of Na current (which is proportional to number of channels open) is positively dependent on magnitude of depolarization
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18
Q

At one point, depolarization causes Na current to decrease
- why is that so?

A
  • depolarization eventually nears ENa— Na driving force into cell decreases
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19
Q

what do the activation/inactivation gate both have in common (think about relationship with voltage) ?

A
  • they are both voltage dependent
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20
Q

what subunit(s) is responsible for modulating NaV channel gating?

A
  • B1/3, b2/4 Immunoglobin-like proteins made of Beta auxiliary subunits
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21
Q

what condition is a mutation in beta1 subunit of Beta1/3 protein of NaV linked to ?

A
  • epileptic seizures
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22
Q

of the 9 NaV Alpha subunits (SNC1A, SCN2A, Nac1.1-1.9) , which subunits are predominant in CNS?
- what common response do they have in relation to TTX toxin?

A
  • NaV1.1,2,3
  • all sensitive
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23
Q

what do Nav1.8,NaV.19 isoforms of peripheral NS (i.e. sensory dorsal root ganglion) have in common?

A
  • resistant to TTX
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24
Q

effect of reduced NaV1.8 expression in mice?

A
  • attenuated neuropathic pain
  • mice lacking 1.8 are analgesic to noxious mechanical stimuli
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25
Q

describe NaV1.7 (as well as result of lack of 1.7) and its role in pain sensing
-what part of body (hint: nociceptive cells)
- NaV1.7 KO effect on inflammatory pain response?

A
  • selectively found in dorsal root ganglion neurons (most in nociceptive cells)
  • TTX sensitive

lack of 1.7 (mice)
- increased mechanical/thermal pain thresholds,
- REDUCED inflammatory pain responses

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26
Q

result of NaV1.7 gain of function mutation (think symptoms of erythromelalgia autosomal dominant disorder)?

loss of function of Nav1.7?

A
  • severe burning sensation, redness in response to thermal stimuli

LOSS OF FUNCTION
- unable to feel pain, acute/chronic

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27
Q

what is the effect of scorpion toxin on grasshopper mouse in terms of pain perception? compared to house mouse?
- why is this so?
- bonus: what is typical effect of venom on NaV1.7?

A
  • Grasshopper mouse is unaffected where house mouse perceives the venom
  • due to venom binding to NaV1.8 and inactivating it— diminished Na current

Venom leads to NaV1.7 activation– pain sensing

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28
Q

properties of Local anesthetics that allow NaV channel blockage (?

A
  • LA´s contain aromatic group that link to basic side chain residue of NaV channel
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29
Q

name of bond formed in Na blockade between Local anesthetic aromatic group and basic side chain

A

Amide/ester bond

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30
Q

what is the blocking action of local LA´s dependent on (think properties of channel/things affecting NaV)?

A
  • USE-DEPENDENT: Drug can only block from inside, hence channel must be in open state
  • VOLTAGE DEPENDENT: depolarization enhances block
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31
Q

effect of Local anesthetics (LA) on Na inactivation process?

A

enhances it

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32
Q

do LA drugs take the hydrophilic or hydrophobic pathway to enter the Na channel?
(note: at phys. pH, LA´s are positively charged)

A
  • trick question—can take BOTH pathways

HYDROPHOBIC– from extracell.
HYDROPHILIC– entering from intracell.

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33
Q

Deletethis card

A
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34
Q

TTX affects neuronal, skeletal, and cardiac NaVs to varying degrees

which channels are blocked by a nanomolar dose of TTX (sensitive) and which ones are blocked by a micromolar (less sensitive) dose?

A
  • neuronal, skeletal NaV: nM
  • cardiac NaV: mM
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35
Q

Residues in P-loop of NaV domains 1-3 contribute to TTX sensitivity

in cardiac cells, what happens when the residue (cystine) responsible for microM TTX sensitivity is mutated to tyrosine (Y)?

note: Y residue is present in P-loop of neuronal channels

in Cardiac NaV P-loop: E,C residues mediate TTX sensitivity

A

Tyrosine mutation greatly increases affinity for TTX

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36
Q

For NaV channels of peripheral NS, what residue is present in the P-loop (same position as Cysteine in neuronal channels) resulting in decreased TTX sensitivity?

A

Serine

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37
Q

what toxin is responsible for paralytic shellfish poisoning and blocks Na at same site as TTX?

A

Saxitoxin (STX)

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38
Q

what toxins, derived from molluscs, are a small positively charged peptide, with toxin version GIIIA selectively blocking NaVs in skeletal muscle (little effect on neuronal NaVs)

A

Micro-conotoxins

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39
Q

what toxins modulate Na channels so that they remain open longer?

A
  • Batrachotoxin
  • pyrethrins
  • b-scorpion toxin
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40
Q

describe batrachotoxin mechanism (poison frogs, bird skin/feather) of action on NaV in terms of
- where it binds from
- effect on channel state
effect on activation voltage

A
  • inhibits inactivation, shifts
  • activation voltage shifted to more -ve potential– channels open longer
  • enters the cell and binds internally
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41
Q

describe Pyrethrin (similar to DDT insecticide) and its mechanism of action in terms of
- where it is derived from
- what organisms it affects
- effect on activation/inactivation

A
  • from plant, natural insecticides
  • non-toxic for mammals, effects insects
  • prolongs activation, inhibits inactivation
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42
Q

describe b-scorpion toxin and its effect on NaV channels in terms of:
- where it binds
- physiolog. requirements for bound toxin to induce effect
- effect on activation

A
  • binds to outer side of IIS4 voltage sensor
  • only becomes effective upon depolarization
  • enhances activation via shifting voltage potential (activation at more -ive potentials)
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43
Q

Describe Sea anemone, a-scorpion toxins effect on NaV channels in terms of:
- where they bind
- effect on gated state and overall activation

A
  • bind receptor site at extracell. end of IVS4 segment (which initiates fast inactivation)
  • normal gating movement of IVS4 prevented— remains in activated/gated state
  • uncouples inactivation form activation
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44
Q

Describe ventricular arrythmia (congenital long QT syndrome) and its characteristics:
- effect on Na current?
- what mutations give rise to these properties?

A
  • prolonged AP duration
  • persistent inward Na current causing abnormal repolarization
  • alpha subunit mutations in NaV1.5
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45
Q

describe Inherited epilepsy syndrome characteristics and mutations that cause it?
- what NaV channels are mutations found in?

A
  • mutations in alpha subunit, some in beta subunit
  • mutations occur in Nav1.1, NaV1.2 subunits
  • MAY induce persistent Na currents
  • mutations may alter voltage dependence of activation/inactivation
    – ENHANCED excitability
46
Q

describe function of CaV channels and cellular events in which they are involved in

A

Intracell. Ca conc. regulation via facilitating Ca entry into cells upon depolarization

CELLULAR EVENTS
- AP generation
- muscle contraction
-NT release
- cell differentiation/ gene expression

47
Q

what are modulators of CaV channels?

A
  • transmitters
  • protein kinases
  • toxins
48
Q

what is the key trigger for fast-evoked transmitter release? (hint: its not K,Na ions)

A
  • elevation of intracell. Ca
49
Q

describe CaV structure
i.e. number of domains, TM segments
- residue present in Pore region
- any auxiliary SU´s?

A

4 repeat domains, 6 TM segments
- membrane associated loop betw/ TM5-TM6 (same as Na)
- Glutamic acid (E)
- Yes

50
Q

Describe L-type (HVA) CaV channels in terms of:
- depolarization amplitude required for opening
- inactivation behavior
- functions
- blockers

A
  • requires large depolarization to elicit opening
  • variable inactivation (may inactivate, may not)
  • E-C coupling, hormone sec., muscle contraction
  • blocked by DHPs
51
Q

Describe T-type (LVA) CaV channels in terms of:
- depolarization amplitude required for opening
- inactivation behavior
- functions
- blockers

A
  • small depolarization (-60 mV) elicits opening
  • exhibits rapid, voltage-dep inactivation (like in NaV)
  • repetitive firing
  • blocked by mibefradil
52
Q

what do N,P/Q, R type CaV channels all have in common?
- compared to L,T type CaV?

A
  • mostly found in neuronal cells (hence role in nt release) whereas L,T are widely expressed in various cells/tissue
53
Q

describe CaV1.1-4 current type and location where it is typically found

A
  • L type
  • cardiac, skeletal muscle, neurons, endocrine cells
54
Q

describe CaV2.1 current type and its location

A
  • P (purkinje)/Q (cerebellar granule cells)
  • nerve terminals, dendrites
55
Q

CaV2.2 current type and location (hint: role in nt release)

A

-N type
- nerve terminals, dendrites

56
Q

CaV2.3 current type and location

A
  • R type (resistant component of neuronal current)
  • nerve terminals, dendrites, cell bodies
57
Q

CaV3.1-3 Current type and location

A
  • T type
  • cardiac, smooth muscle, neurons
58
Q

differences between A1 CaV SU and Na channel SU?
- think in terms of domains, TM segments in each domain, linker loop

A

trick question: no difference, A1 subunit is structurally same as NaV one

59
Q

describe beta subunit of CaV channel in terms of:
- location
- whether there is a specific number of b Su associated w/ A at a time

A
  • intracellularly located
  • there can be multiple b subunits associated w/ 1 A
60
Q

describe glycosylated A2, Delta SU (component of CaV) in terms of:
- function
- location
- associations

A
  • found extracellularly; A2 attached to membrane via Sulfide linkage w/ delta SU
    – Delta SU anchors A2 w/ A1
61
Q

Describe Gamma (Y9) glycoprotein in terms of:
- structure
- genetic makeup
- function

A
  • 4 TM segments
  • 8 genes encoding for it
  • function unclear
62
Q

L-type CaV channels display mode switching i.e multiple gating kinetics.

  • describe the 3 different kinetic modes
A

Mode 0– no channel openings
Mode 1– brief channel opening state
Mode 2– prolonged channel opening

63
Q

in what way do catecholamines modulate current of CaV1 channel family in the heart?
- consider consequences in terms of inotropic action (muscle contraction)

A

Catecholamines modulate CaV1´s via phosphorylation– enhance Ca current
– underlies positive inotropic action

64
Q

in what way do beta-adrenergic agonists modulate CaV1 (L-type) channel activity?
- consider effect on AP amplitude (i.e. muscle contractility/rate)
- what kinetic mode is induced?

A
  • CaV1 phosphorylation by agonist
  • increased AP amplitude, contractility/rate
  • mode 2 induced
65
Q

what second messenger mimics the effect of beta-adrenergic stimulation of CaV1 channels through PKA activity?

PKA leads to phosphorylation of which residue (at what site?) of CaV1.2?

A
  • cAMP
  • Ser1928
66
Q

effect of B2a SU on b-adrenergic agonist activation of CaV1.2?
- what residue site implicated?

A
  • enhanced b-adrenergic agonist activation of CaV1.2
  • phosphorylation of Ser478/479
67
Q

Difference between CaV1 and CaV2(P/Q,N) regulation?

A
  • CaV1 is regulated by kinases/phosphorylation
  • CaV2 regulated by G-protein coupling
68
Q

result of G protein coupling on CaV2 Ca current?
- effect on synapt. transmission?
- effect on Ca entry at nerve terminal?

A
  • inhibition via local membrane action
  • decreased synaptic transmission
  • reduced Ca entry
69
Q

type of inhibition caused by G protein beta/gamma dimer?
- (bonus: where else do we see beta/gamma GP dimer inhibit Ca entry?)

A
  • tonic inhibition
  • presynaptic GABAb receptor
70
Q

what mechanism reverse G-Protein tonic inhibition of Ca current?

A
  • Depolarizing prepulse
71
Q

issues related to A1 KO in CaV1 (L-type) family?
(hint: think about location in which they are found)
- blockers of CaV1?

A
  • cardiac, skeletal, dysfunction– endocrine as well

phenotypes: cardiac arrythmia, deafness, weak muscle contraction
- DHPs

72
Q

issues related to A1 KO in CaV2.1 (P/Q) family?
blocker?

A
  • pain hyposensitivity
  • agatoxin IVA
73
Q

issues related to A1 KO in CaV2.2 (N) family?
(bonus: describe effect of baclofen on mutant N type CaVs)

A
  • pain hyposensitivity
  • resistant to baclofen induced seizures
74
Q

issues related to A1 KO in CaV3 (T) family? (remember: T types expressed in cardiac, smooth muscle (Cav3.3 exception– in neural tissue))
blocker?

A
  • compromised vascular function
  • blockers include kurotoxin (3.2 is blocked by nickel)
75
Q

Mechanism of Dihydropyridine (DHP) antagonists in L type CaV inhibition?
- what kinetic mode do they encourage?
- effect on gating behavior?

A
  • allosteric modulators (gating behavior altering)
  • stabilize mode 0
76
Q

what is nifedipine and describe its effect on L type CaV channels
- i.e. what kinetic mode does it encourage?

A
  • CaV1 agonist– stabilizes mode 2
77
Q

what are the 3 major classes of L- type CaV channel antagonists

describe their clinical uses.

what happens if they bind the same site on channel (note: will still cause blocked Ca influx) ?

A
  • DHps
  • PAAs (verapamil)
  • Benzothiazepines (diltiazem)

treatment of hypertension, cardiac arrythmia, ischaemic heart disease

  • binding of same site will induce different effects/ mechanisms of blockage
78
Q

location of binding site of DHPs
(hint: particularly TM segments in domains III-IV, I as well)

A
  • S5,S6 TM segments of A1 SU
79
Q

what region are these DHP sites found in?
- Y1485
- M1486
- I1493

A
  • S6 TM segment of domain IV (aka IVS6)
80
Q

describe phenylalkylamines (PAAs) L-type CaV blockage mechanism in terms of:
- location of binding
- conditions of effect (voltage/use dep/independent?)–

bonus: what antagonist of Na channel shares similar action i.e use dep

A
  • intracellular binding— inner end of TM pore i.e domain III-IV S6
  • Ca blockage is USE-DEPENDENT– open channel block
81
Q

action of benzothiazepine antagonists on L-type CaV channels?
- location of binding

A
  • act extracellularly
  • bind residues of Domain IV S5-S6 linker
82
Q

Toxin that interacts with N type CaV
- causes chronic neuropathic pain

A

Ziconotide

83
Q

mechanism of gabapentin/pregabalin in treatment of epilepsy, chronic pain?

A
  • interaction with A2delta subunit of CaVs
84
Q

describe Type 1 hypokalemic periodic paralysis, a CaV1.x channelopathy, in terms of:
- what CaV channel (hint: L-type) it effects
- location of mutation (hint: voltage sensor segment)
- consequence of mutation

A
  • CaV1.1 in skeletal muscle
  • S4 segment
  • reduced Ca current– muscle weakness
85
Q

describe Timothy syndrome in terms of:
- what CaV channel (hint: L-type) harbors mutation
- consequence of mutation

A
  • CaV1.2 mutation
  • loss of inactivation (i.e. inc. Ca entry) —> cardiac dysregulation
86
Q

describe Night blindness channelopathy in terms of:
- what CaV channel (hint: L-type) it effects
- consequence of mutation (hint: think NT release at retinal photoreceptor terminals)

A
  • multiple mutations associated with loss of CaV1.4 function
    –decreased NT release from retinal photoreceptor terminals
87
Q

what CaV channel mutations are familial hemiplegic migraines linked to(hint: non L/T type,and affects nt release)?
- consequences of mutation?

A
  • CaV 2.1 (P/Q)
  • increased channel activity, NT release
88
Q

describe ATAXIA type 2 channelopathy
- what CaV channel mutated (hint:non L-type)
- consequences of mutation

A
  • CaV2.1 gene disruption
  • cannot form functional channels
89
Q

describe epilepsy channelopathy and their effect on P/Q CaV function
- what SU´s mutated

A
  • auxiliary subunit mutations
  • Ca channel misfunction
90
Q

describe autism channelopathy
- channels implicated
- bonus: what might parents of autistic child suffer from

A
  • CaV3.2 (T type)
  • parents might suffer from epilepsy– Ca channel misfunction
91
Q

what V-gated ion channel is most diverse genetically and in terms of physiological function?

A
  • Kv channels
92
Q

Kv channel regulate what physiological functions

A
  • cell volume control
  • Vm/excitability control
  • salt, hormone, NT secretion
93
Q

intrinsic/extrinsic factors in which Kv channels are regulated?

A
  • hormones/NTs
  • kinases, phosphatases
  • G proteins
  • Ca/ATP conc. in cytoplasm
94
Q

what K channels consist of 6 transmembrane segments?

A
  • Kv channels
  • hERG channels
  • Ca activated K channels
  • KCNQ channels
95
Q

in the ball and chain model of ´A´ type Kv channels, what AA residues form ball/ chain that mediate fast inactivation?

A

BALL– first 20 amino acids form hydrophobic/charged surface domain
CHAIN– the following 50-60 AA´s

96
Q

characteristic of ´A´ type Kv channels?

A
  • rapid inactivation following opening of channel
97
Q

by what interaction mechanism does “ball” component of Kv channel lead to inactivation?
hint: think of terminal

A
  • N type/ N terminal structure involvement facilitates Kv inactivation
98
Q

3 Ca activated Kv and their location

A
  • Large conductance (maxi-K) – 250 pS– ubiquitously expressed (except in heart)
  • Intermediate conductance channels– 60-100 pS
  • Small conductance (SK)– <20 pS– function in neuron in AHP mediating
99
Q

as Maxi K activation voltage is not fixed (dependent on intracell. Ca conc), what is the effect of increasing Ca conc. on Maxi-K channels?

A
  • as intracell. Ca increases, electrical energy required for channel opening is reduced
100
Q

given that Maxi-K alpha subunit is encoded for by single gene (slo) what is the reason for Maxi-K diversity?

A
  • alternative splice exons in maxi-k gene
  • accessory beta subunits interacting w/ alpha SU
  • S0/N-terminal domains; needed for beta SU channel modulating
101
Q

in what Kv channels is the Alpha subunit primary sequence found?
bonus: in what Kv channels is S0 terminal domain found?

A
  • primary sequence is homol. to ALL Kv channels (trick question)
  • S0 found only in maxi-k channels
102
Q

describe the two independent sensing mechanisms of Maxi K channel (Voltage sensors, ligand gating mechanism)

  • what segments make them up?
A
  • Voltage sensor; made of S4 TM segment of alpha subunit

Ligand gating mechanism
- made of hydrophobic domain S7-S10
- S7-S8 is RCK (regulator of K conductance) domain
S8-S9 linker makes tail domain

103
Q

effect of intracellular ring (RCK domain) on S4 (voltage sensing) upon Ca binding?

A
  • Ca binding to intracellular RCK domain leads to expansion– acts on S4 gate, channel opens
104
Q

what characteristic of A1 SU Tail domain makes it capable of being Ca sensitive?
- what would its mutation do to Ca sensing?

A
  • D residue between S9-S10
  • affect high affinity sensing
105
Q

effect of increasing intracell. Ca conc. on RCK domain and overall channel gating?

A
  • more Ca binding to RCK–> interacts with Ca bowl/tail –> greater force of channel opening
106
Q

relationship between increased opening force on channel gates via RCK binding and S4 driven conformational change of Maxi-K channel?
i.e. which one depends on which?

A
  • trick Q: they are INDEPENDENT of one another
107
Q

describe physiological roles of Maxi-K

A

-cochlear hair frequency encoding
- opposes vasoconstriction by inducing hyperpol. in smooth muscle
- contributes to AHP i.e. refractory period

108
Q

what class of K channels is most abundant
- hint: 4TM/2P family
ex. TWIK, TRAAK, TREK, TASK

A

K2p weak inward rectifiers

109
Q

describe TREK1 (of K2p channel family) in terms of
- number of P loops
- state of channel at rest

A
  • 2 P loops
  • constitutively open at rest
110
Q

what two ion channels mediate bursting pacemaker activity?

A
  • CaV channels
  • Ca activated K channels

Biomembranes (8 decks)

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