Ion channels

what is selectivity?

Based on the dominant ion that moves through the same pore. Eg Na, K, Ca and cation non-selective Based on the ion that moves through the pore, classic way of classifying the channel

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in the last 20 years what have they started to identify calcium channels on?

their molecular structure- based on the sequence of amino acids in the protein that makes up the ion channel and classifying ion channels into family groups based on similarity

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what is gating?

gating refers to the open and closing of the channels. Some ion channels are voltage gated, ligand gated, regulated by signalling pathways

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what are voltage gated channel examples?

VG = their open probability changes with the membrane potential- lots of examples of these very common in electrically excitable cells

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what does the ligand gated channels open probability change with

open probability changes with the binding of a ligand to a specific binding site on the channel

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what is a K example of being regulated by signalling?

ATP sensitive K channels- regulated by ATP inside the cell

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what is an example of a mutation in ligand gated ion channels?

hyperekplexia

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what do we classify ion channels based on?

selectivity, gating and their molecular structure

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what is conductance measured in?

siemens- usually nano or microsiemens

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what is 0.03723404 to 2dp?

0.04

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examples of selectivity?

eg Na selective, K, chloride selective channels or cation non-selective so they let many different cations through

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2 types of gating?

1) voltage gated 2) ligand gated

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what changes with the membrane potential in the voltage gated channels?

their open probability changes with the MP

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where are voltage gated channels commom?

electrically excitable cells

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what is voltage dependent gating?

open probability changes with the MP. Channels could be opened by depolarisation/hyperpolarisation and depol/hyperpol causes them to close

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VG gated channels?

K, CLC chloride channel, Na and Ca VG channels

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examples of channels that are opened by the binding of a ligand?

nicotinic acetylcholine receptor, glycine rec, P2X receptors

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what happens when acetylcholine binds to the nicotinic acetlycholine receptor?

ach binds opens up the channel which is a cation channel which lets Na and Ca through

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what are P2X recs opened by?

binding of ATP at the EC AP-ligand binding site, they open and let ca into the cell

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what can you be gated by if you're not gated by the MP or ligand gated because they don't have a binding site for a ligand?

regulation by signalling pathway

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what are recs that are gated by signalling pathways?

Kir inwardly rectifying K channel family and CFTR

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what are recs gated by signalling pathways regulated by?

phosphorylation, G proteins, calcium kinases, phosphatases- complex pathways regulate signalling

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what subunits is the VG K channel made up of?

made up of subunits that consist of 6 TM spanning domain. 4 of these subunits come together to make a functional channel. pore region, 4 of them come together to make the pore of VG K channel

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what is a TM spanning domain? what would you get if you had 6 TM spanning domains?

TMDs- the sequence of amino acids that span the membrane itself so 6TMDs 5 points where protein spans the membrane

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what happens if there is a mutation in any of the 4 subunits of the VG K channel?

mutations in 1 of the 4 subunits can stop the whole channel from functioning = dominant negative effect

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what is the pore region?

the sequence of amino acids that come together to make the pore- aa here are really important in determining the selectivity of the channel

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where is the S4 region in the VG K channel?

TMD 4

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what is the S4 region?

the region that is the voltage sensor in voltage-dependent K channels

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how many subunits are needed to make 1 K ion channel?

4 of these subunits

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what is the Kir channel?

inwardly rectifyining. Its K selective

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what is the structure of Kir?

2 TM domains. There is no voltage sensor as they are not voltage dependent. Have a pore region between TMDs 1 and 2. 4 of these come together to make a functional Kir channel. Have 4 aa seqs that come together to make the pore that lets K thro

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how is Kir similar to Kv?

they are both selective for K, they both need 4 subunits to make the functional channel

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structure of VG ca and Na channel?

one gene product that has 24 TMDs in 4 blocks of 6. Got 4 pore regions and again this is the sequence in the pore region that determines selectivity. S4 reguon of 4 TMD in each of the 4 blocks of 6

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how is VG Na and Ca channel similar to Kv?

Kv we have a subunit with 6 ™ spanning domains and we need 4 of them and that’s essentially the same as having one protein that has 24 ™ spanning domains

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what channels have beta subunits?

Na, K, Ca, CLC chloride channels

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what do beta subunits do?

regulate the ion channels- are usually smal;l MW proteins that regulate lots of different properties of the main ion channel

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what are the ion channels called?

alpha subunits

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how many TMDs does Cav have?

24

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how is Cav like Nav?

has 24 TMDs, 4 lots of 6, 4 pore regions and 4 voltage sensors all like Nav

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how do we know Ca and Na channels are really similar?

if you take Na channel and mutate certain aas in the pore you can turn it into a ca channel so there's lots of structural similarities- really specific aa in pore regions that determine if Na or C achannel. Just 1 aa diff in 1 of 4 pore regions na-ca

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why does the number of channels change the current?

increase hte number of channels increase the current flow, devcrease num of channels decrease the current

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what does a open probability of 0 or 1 mean?

0- channels closed all the time to 1-oepn all the time. The higher the open probability the more often the channels are open the bigger the currents

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what is single channel conductance a measure of?

a measure of ions moving through the pore per unit time- is essentially a constant

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what is the driving force for ion movement?

MP - NP the difference between the membrane potential and nernst potential

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the further away your MP is from the nernst the what?

bigger the driving force, the bigger the currents you're going to record

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how do you change the number of channels in the membrane?

by membrane shuttling- insert/remove channels

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what can open probability be changed by?

MP, ligand binding and 2nd messengers eg ATP, G proteins, ATP, Camp and phosphorylation.

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if you change the MP what will change?

the driving force

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what would a change in MP come from?

the activation or inhibition of other channels then this changes the driving force for ion movement

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what techniques do we use to clamp the MP?

patch calmp technique or the 2 electrode voltage clamp technique

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why do we use these techniwues?

so we can clamp the MP and determine exactly what the DF is and then we measure the ion flow

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what does the 2 electrode voltage clamp technique do?

it clamps the potential at the value you want and then you can measure the current flow across the M. Clamp to diff potentials and measure the current.

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what would an IV curve for a channel that is not voltage dependent look like?

straight line

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what does it mean if a channels not voltage dpeendent?

the membrane potential is not changing the open probability. The open probability is fixed at the MP.

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on the IV curve what goes on the X and Y axis?

X = voltage (mV) Y= Current (pA)

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what is Vrev?

the potential at which there is no net movement of ions through the pore of the channel. So it doesn't mean there isn't any ions moving it means the ion movement in one direction is balanced by ion movement in the opposite direction

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if you open an ion channel what do you drive the MP towards?

the nernst potential for that ion

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if you open an ion channel the Vrev will be close to whqat?

the nernst potential for that ion

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if the Vrev is close to the nernst potential for an ion what does thsat mean?

the currents are probably mediated by that ions channels

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if the reversal potential is very positive what currents is it likely to be?

Na

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if the reversal potential is very negative what currents is it likely to be?

K or chloride

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having a smaller driving force does what to the currents?

means currents will be smaller

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what do negative and positive currents reflect?

the direction that the majority of ions are moving

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Any potentials that are more positive than your reversal potential will give you what?

positive currents

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Any clamped potentials that are negative to your reversal potential will always give you what?

negative (inward currents)

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the bigger the difference between what determines the size of the currents?

the clamped MP and Vrev. The bigger the difference the bigger the currents you will record

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what does a straight line IV curve mean?

this channel is not voltage dependent and there is no change in the open probability with the membrane potential.

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what are positive currents called (above 0 on graph)?

outward currents

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what are negative currents called (below 0 on graph)?

inward

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what is the profile for outward rectification?

really big outward positive currents and much smaller inward negative currents

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why would we see outward rectification?

voltage dependence of open probability- you'd have an ion channel whose open probability got bigger and bigger as the MP shifts in a more positive direction

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whats the characteristic profile of inward rectification?

inward negative currents are much bigger than outward positive currents.

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why would you have inward rectification?

voltage dependence of Po or in Kir K channels this is caused by a magnesium block of the pore which prevents some of the outward flow of K

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how did they come out with defining inward and outward currents?

Neyer and Sachman came up with a convention based on physics principles that defined them

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what did they define positive outwards currents as?

cations moving out and anions in

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what did they define negative inwards currents as?

cations in and anions out

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why do anions and cations have to move in opposite directions?

+ve ions moving out generating a +ve and outward current if you’ve got anions they’ve got to move in the opposite direction to generate the same positive current because they have a negative charge.

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what does each line on a current recording thing mean?

each line represents the current recorded at a different clamped potential

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why would the gaps between the lines get bigger and bigger as the MP becomes more positive?

voltage dependence- the channel is activated by depolarisation. It's a voltage dependent ion channel so every time the MP is shifted more +ve the Po is going up- channels opening more often so currents get bigger

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whats getting bigger at higher clamped potentials?

the driving force + the open probability

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why would we want to quantify the voltage dependence?

if you've got a mutation in an ion channel implicated in a disease and we think it impacts on voltage dependence we want to analyse it statistically so got to quantify it

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how do we overcome the fact that we have changes in Po and driving force to just quantify voltage dependence?

calculate the point conductance and then plot it against the potential

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what do you do to see voltage dependent gating?

calculate conductance, plot conductance against voltage, model to boltzman equation

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what can you read off the G vs Voltage graph?

Vo = the voltage when the conductance is 50% w= the gating charge

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what is the gating charge (w)?

a measue of how steep the relationship is between the potential and G/Gmax

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what is the Vo?

the potential when the conductance is 50% of the maximum conductance so its the potential where the channels are open for half the time

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how do they usually get the Vo?

by mathematically modelling it but can find it from the graph

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why is the Vo useful?

know in WT when half channels are maximally activated/open do the same experiment with mutant channel and see if you get the same vo value. Shows impact of mutation on voltage dependence

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what does it mean if the Vo of the WT and mutant is the same? different?

if it's the same as the WT it means voltage dependence is normal. If its different voltage dependence is changing bcos of the mutation

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what could you plot instead of the G/Gmax?

the open probability- if you did single channel recordings and knew what the open probability was could plot this against MP to get vo value

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what structures underlie voltage dependent gating?

S4 regiion and the ball and chain region

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what channels is the S4 region found in?

the Kv Cav, Na, so voltage gated channels

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what does the S4 region do? what does it have in it?

is the voltage sensor- has oltage sensing aas that determine the voltage dependence of activation

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how is inactivation more complex?

MP opens the channel and channel will close with MP eg Na channel in the AP but clsoing is mediated by ball and chain mechanism

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what forms the ball and chain in Nav and Cav?

3-4 linker region. This is a sequence of aas between the 3rd set of 6 TMDs and the 4th set of 6 TMDs

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what is the ball and chain?

a sequence of aas that forms a ball with a chain that connect it to the protein (so part of the protein itself)

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when does the ball and chain operate?

going from open to inactivated is the little ball of aas popping into the pore and blocking it

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what must the channel do to open again? what does this determine?

go from inactivated to closed to open again- this is what the refractory period is in terms of activation of VG Na channels. They wont open again unless inactivated t closed and this is mediated by ball and chain

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what do blockers do to the current?

makes the current smaller

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what do blockers do to: 1) positive currents? 2) negative currents

make them smaller so 1) positive direction fown closer to 0 2) negative value up closer to 0 = currents get smaller across all potential ranges

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where is pro-Txx II from?

taruntala venom

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what happens with Pro-ttx-II?

large inward currents get smaller and smaller with the blocker so currents decrease. Loss of inward current- less cations moving in (or anions moving out)

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what does pro Tx-II inhibit?

VG Na channels- less Na moving into the cell

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how do we work out conductance of particular currents?

ohms law. Rearrange G= I/V. Measure currents divide by the potential

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why is it called a chord conductance?

it doesn't sit directly over the data

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are blockers specific?

no blocker is 100% specific they always block things you don't expect them to

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how many individuals affected by syncope and sudden cardiac death a year?

1 million over Europe and America

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some of these are caused by what?

ion channel mutations

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what is Timothy's syndrome usually classed as?

can be classed as LQT but sometomes classed as a separate syndorme- classification weird

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what is the caridac Ap 1) depol phase 2) plateau phase and 3) repol phase mediated by?

1) depol VG Na channels 2) Plateau phase- VG Ca channels 3) repol- VG K channels

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structure of Cav?

1 alpha subunit that forms the whole channel- 24 TM domains, each subinit forms one functional channel. 4 voltage snesors. 4 pore regions, regulatory beta subunits

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what are the types of Ca channels? what were they characterised by?

L, N, P/Q, R and T type ca channels- characteristised by sensitivity to MP

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whats the gene for Cav1.2?

CACNA1C

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where is Cav1.2 found?

in the heart, brain and lungs

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what type of ca channel is Cav1.2?

L type high voltage gated

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how many alternative splicing locci does Cav1.2 have? what does this mean?

12 alternative splicing locci- means when the channel is constructed the 24 subunits are put together different combos of aa seqs so there's the potential for 42 different splice variantrs to arise from 1 gene

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how many different versions of Cav1.2 can we have becausde of the spliced variants?

42 versions

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where are cav1.2 channels in muscles found?

in t tubules close to the sacroplasmic reticulum

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what kind of inactivation do Cav1.2 channels have?

voltage and ca dependent inactivation

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why does the current curve steepen out with Cav1.2?

all the channels have opened so have maximum current

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what is generated by ca moving into the cell?

inward and negative current is generated

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what is inactivation dependent on for Cav1.2?

MP and is accelerated in the presence of calcium

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what does high ca at the IC surface di?

promotes activation and there's a voltage dependence too

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what is inactivation of Cav1.2 regulated by?

the beta subunits- have the ability to shift the voltage dpeendence, important as mutations in beta or alpha subunits change function

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what is mutated in Timothy's syndrome?

Cav1.2

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why do we say Cav1.2 is altered rather than mutated in Timothy's syndrome?

because the mutation will only be in some of the spliced variants not all of them

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what organs are affected in Timothy's syndrome?

heart, skin, brain, teeth and eyes

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what is the symptoms of Timothy's syndrome?

have congenital heart disease- demonstrate arrhythmias, syndactly (fused digits), immuine deficiency, autism, round face, flat nasal bride, thin upper lip, webbed jaw, nose doesn't project out

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what is prolonged in the heart of a person with Timonthy's syndrome?

have a severe QT prolongation

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what is Timothy's syndrome a form of?

Long QT syndrome

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what does a corrected QT interval take into account?

QT interval taking into consideration the heart beat so the duration of the cardiac cycle

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is Timothy's syndrome inherited?

yes

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what do you characteristically see on an ECG with Timothy's syndrome?

2:1 AV block + a severe prolonged QT interval + alternating T wave polarity

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what is a 2:1 AV block?

have 2 P waves to each QRS complex. P wave is atria depol so atria depol but ventricles can't respond as they haven't finished responding to the first attria depol. A signal from the atria depol stops and its blocked can't get into ventricles block o

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what does a 2:1 AV block make you at risk of?

arrythmias as timing all over the place

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what is alternating T wave polarity?

see a positive t wave then negative then positive then nehgative t wave

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what does it mean if you see alternating T wave polarity on an ECG?

there is severe cardiac repolarisation defect = becuase there's a prolonged QT internal

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why is a prolonged T interval a problem?

it starts to disrupt all the electical signalling in the heart

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what happens if you have a prolonged QT interval and you increase their heart rate?

go into ventricular tachycarida- significant risk of cardiac death

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what is ventricular tachycardia?

lots of uncoordinated contractions of the ventricles

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out of 17 children who started the Timothy's study how many of them died during the study? what does this show

10 of them-born with Timothy's syndrome = high risk of death, not a good prognosis in terms of survival

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what else did this study show?

12/17 experienced life threatening arrythmias so they're common, had motor + cognitive impairments. In the brain have a wider impact and have autism

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why is Cav1.2 altered in Timothy's syndrome and not a mutation?

the mutation is in a gene that does not always end up in the protein- spliced variants - only a small selection of Cav1.2 protein is diff bcos of spliced variants

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they looked at 13 patients and found a shift in what position?

position 406

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what was the change at position 406?

glycine to arginine-

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why is this aa acid important?

it is usually conserved usually all of the spliced variants have got glycine at 406, conserved in most animals and in most ca channels

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in Timothy's syndrome some of the spliced variants turn glycine at 406 to what?

arginine

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is the VD inactivation or Ca dependent inactivation affected in the G406R mutant?

the VD inactivation

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why does the ca current start going up again?

at this potential is pushing the ca off it's binding site allowing the channel to open up again so it's relief of the ca dependent inactivation.

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main impact of G406R mutation?

bigger currents because inactivation is slowed- more calcium current is left

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how did they get rid of calicum dependent inactivation so they could just look at voltage dependent inactivation?

used barium as it would still generate currents but wouldn't act back and inactivate the channel like calcium ions do

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what other thing is barium used for other than a replacement for ca channel ion?

K channel blocker

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what did they find when they just looked at VD inactivation with barium currents?

WT normal, but mutant inactivation is almost completely gone

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why is this different to when there's ca dependent inactivation?

before ca was making it inactivate a bit so had some inactivation but now looking at just VD and VD inactivation is gone

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what is the impact on Cav1.2 channels not inactivating in the ventricular mycoytes?

plateau phase is maintained for longer, open but VD is altered so they stay open because they're not inactivating so as the MP depol ca channels stay open for longer. Plateau phase is prolonged so delay repolarisation in patients = LQT syndrome

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why do we have LQT in TS patients?

Cav1.2 channels don't inactivate when they should

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why are not all the Cav1.2 channels affected?

shift/change in the aa sequence is only seen in some of the spliced variants- estimate 11.5% of the channels in the patients cells are affected

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why is it such a small amount 11.5% but it has such a big impact by giving a mean death age of 2/5yrs?

predict that the cardiac APs are about 17% longer that extension is sufficient to cause the problems we see in the patients in terms of arrhythmias the 2:1 AV block and the issues of sudden cardiac death in these infants. only 11.5% still huge impact

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summed up what less inactivation of Cav1.2 results in?

prolonged plateau phase -> delay repol -> extend cardiac AP ->arrythmias -> 2:1 AV block -> sudden cardiac death

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what is the SQT syndrome we looked at where there's a shortening of the plateau phase?

Brugada's syndrome

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how many types of Brugada's syndrome is there?

5 subtypes. Ikr and Iks currens.

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Brugada's syndrome is GOF in what?

K channels

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what does the GOF K channel mean?

repolarisation speeds up = short QT syndrome

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Brugada's syndrome is a LOF in what?

Cav1.2

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Cav1.2 LOF in Brugada's syndrome is what type?

short QT type 4 + type 5 is a LOF in the beta subunit B2b which regulates the Cav1.2 alpha subunit

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what do you see on the ECG with Brugada's syndrome?

accentuated J wave and ST segment elevation + short QT interval

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where is the J wave usually seen?

at the end of the QRS ocomplex- tiny in a normal individual

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what is a short QT interval defined as for a male and female?

male- bleow 350ms, female- below 370ms

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where did the patients they looked at have mutations?

2 in ca channel itself: 1) 490 glycine -> arginine 2) 39 alaine -> valine 3) 481 in beta subunit serine -> leucine

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what could be giving the decrease in currents if the activation + inactivation is normal?

shift in VD or a decrease in the number of channels

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what was seen with all 3 mutations?

smaller currents (ca currents)

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why could having a mutation in the beta subunit have an impact on how Cav1.2 function?

The beta subunits play a really important role in helping determine the voltage dependent inactivation of the calcium channel

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what is the difference to the VD in the mutant and to the currents?

VD is the same is just the ca currents are smaller

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what do the downward plot points show?

change in DF + Po

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what do the upward points show?

change in DF

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what does having smaller ca currents do to the cardiac AP?

you don't have a plateua phase

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why might there be smaller currents?

changes in VD or changes in the number of channels- VD doesn't look different with mutations so must be change in ability of channels to open

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was the location of WT Cav1.2 the same as G509R and S481L mutations?

yes both found at the CM and inside the cell

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what does this mean?

unlikely to be a trafficking mutaiton

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what did they think was happening to these 2 mutations to give smaller ca currents?

the pore of the channel is not working properly so the channels have similar VD but the pore itself not opening fully to let ca ions thro

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what did they find with the location of the A39V mutation?

its found perinuclear- diff to WT.

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what does this mean the A39V mutation is likely to be cause?

reduction of current becuase there's a reduced number of channels at the membrane

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structure of VG Na channel?

24 TMDs, 4 voltage sensors, 4 pore regions come together to make the actual pore of the channel

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what are beta subunits?

tend to be small MW, they regulate the properties of ion channels

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what kind of things do beta subunits regulate?

gating, voltage dependence, regulation of signalling pathways, sensitivity to drugs

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what channels ahve beta subunits?

Cav, Kv, Kir, Cl

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long QT affects what cell?

ventricular myocytes

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what happens at the peak of the cardiac cell action potential?

Na channels close and VG channels open and they take longer to open than Na channels but they maintain the plateau phase

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what dictates depol, plateau phase and repol?

depol-Nav, Plateau- Ca, repol- K

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what part of the AP are we interested in in long QT?

VG K channels in the repol phase

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any impact on K channels will delay what?

repolarisation- if mutation in one of the 2 channels it's not that repol doesn't occur it just takes longer

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why was hERG1 names the way it was?

human erythrogogo- when mutated fly did funny dance in respond to ether

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what is the gene for hERG1?

KCHNH2

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what current does hERG1 underlie?

Ikr current

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characteristics of hERG1?

rapid activation (slower than Na but faster than Q1), 1 of the first channels to drive repol, rapid inactivation, inward rectification, delayed rectifier

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why is it a delayed rectifier?

it demonstrated rectification but there is a delay in timing, the timinf of the oepning of hERG2 is delayed in comparison to opening of Na + ca

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gene name for Q1 (KvLQT1 channel?

KCNQ1

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what current does the Q1 current underlie?

Iks currents

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what channels are needed to mediate the Iks current?

Q1 and E1 (beta subunit)

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characteristics of Q1?

important in driving repol, slowe activation than herg channels, outward rectification as its VD is opened by depol, PO increases as potential more positive currents get bigger, delayed rectifier, regulated by E1

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why was E1 first called mink?

they thought it was a K alpha subunit in its own right- overexpressed in xenopus oocyte cells they had really big K currents thought there was more K channels why current were bigger

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how many family members of the KCNE b subunit family are there?

5

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how many aas are KCNE family like E1?

129-130 aas, one TMD, physically interacts with Kv to regulate its properties

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