Electrical Excitability

Question 1

What happens when the conductance of any ion is increased

Answer 1

The membrane potential will move closer to the equilibrium potential for that ion

Question 2

What determines the conductance of an ion

Answer 2

Dependant on the number of channels for the ion that are open

Question 3

What is the relationship between axon diameter and the increase in sodium ion concentration needed for depolarisation

Answer 3

As the axon diameter increases the concentration decreases. Easier to fire an action potential

Question 4

What happens in the absolute refractory period

Answer 4

Nearly all sodium channels in the inactivated state

Question 5

What happens in the relative refractory period

Answer 5

Sodium channels are recovering from inactivation. The excitability returns towards normal as the number of sodium channels in the inactivated state decreases and potassium channels close

Question 6

Basic structure of voltage gated sodium channel

Answer 6

One alpha subunit which consists of 4 similar sections or repeats

Subunit 4 contains positively charged amino acids which can experiment an electrical field as they are within the membrane. Membrane potential can impose a force on these so when there is a stimulus they detect it and open or close the channel

There is also an inactivation particle

Question 7

Basic structure of potassium ions

Answer 7

A functional channel composes of 4 alpha subunits

Also have the positive transmembrane segment

Question 8

How do local anaesthetic work

BH- charged local anaesthetic
B uncharged local anaesthetic

Answer 8

Open channel block, or hydrophillic pathway- block sodium ions from moving through the channel

Hydrophobic block pathway- block sodium channels in the inactivated state

As pain fibres open they are more susceptible to bein blocked by the BH-

Question 9

What order do local anaesthetics block

Answer 9

Small myelinated axons

Unmyelinated axons

Large myelinated axons

Question 10

Why is important that sodium channels become inactivated

Answer 10

Enables the repolarisation to occur quickly, also because when they are inactivated they cant open again leading to the refractory period

Question 11

What is the consequence of the delayed closing of voltage gated postasium ions

Answer 11

Ensure hyperpolarisation as it makes sure the inside f the cell is negative enough to ensure quick recovery of sodium channels from inactivation

Question 12

Why is the NA/K ATPase not involved i action potential

Answer 12

There is little flow of ions to change the membrae potential

Question 13

Define capaticance

Answer 13

ability to store charge

a low capiticance is ideal for faster conduction

Question 14

What is membrane resistance

Answer 14

depends on the number of ion channels open. The lower the resistance the more ion channels are open.

Question 15

What does high capaticance/ resistance cause

Answer 15

Capaticance- voltage changes more slowly in response to current injection into an axon

Resistance- change in voltage spreads further along the axon

Question 16

Effect of myelin on the length constant

Answer 16

Increases as it is a good insulator, it enables the local circuit current to depolarise the next node or ranvier above threshold and initiate an action potential

AP jumps from node to node allowing faster conduction velocity

Question 17

Action potential propagation

Answer 17

• an action potential causes depolarisation of adjacent sections of the axon
• where this local depolarization reaches threshold an action potential is initiated
• the spread of this local change in the membrane potential is increased by a high membrane resistance and low membrane capacitance – the longer this distance the faster the conduction
• myelinated axons have a high membrane resistance and low membrane capacitance

• the action potential jumps from node to node – termed saltatory conduction, which is faster than
that in unmeylinated axons

• damage to the myelin (e.g. in multiple sclerosis) can stop saltatory conduction

Question 18

Why does calcium influx have such a great effect

Answer 18

Because the concentration of Ca2+ inside is so low, the Ca2+ influx through Ca2+ channels can raise the internal concentration of Ca2+ significantly.

Question 19

Structure of voltage gated calcium channels

Answer 19

Similar to sodium channels

Question 20

Transmitter release

Answer 20

1. Ca2+ entry through Ca2+ channels
2. Ca2+ binds to synaptotagmin- brings vesicles close to membrane of the nerve terminal
3. Vesicle brought close to membrane
4. Snare complex make a fusion pore 5. Transmitter released through this pore

Question 21

What is a snare complex

Answer 21

Neurotransmitters fusing with membrane

Question 22

NAChR

Answer 22

Nicotinic acetylcholine receptor

Ligand acted ion channel

Permable to cations

Question 23

What is end plate potential

Answer 23

Depolarisation occurs as the resting membrane potential is quite negative [-90mv] close to potassium equilibrium potential but far away from the sodium equilibrium potential. There is a large electrochemical gradient for sodium to move into the cell and potassium out. This is why when ACh binds and opens the channels there is depolarisation

Question 24

What is neurotransmitters release dependant on

Answer 24

Ca2+ entry

End plate potentials decrease in amplitude as external ca2+ is lowered

Question 25

What causes local spread of charge in the muscle

Answer 25

Brief depolarisation will activate adjacent Na+ channels due to local spread of charge causing a muscle AP

The AP then initiates contraction of the skeletal muscle fibre this is excitation contraction coupling

Question 26

Competitive block by d-TC

Answer 26

The d-TC binds competitively to nAChr blocking ACh from binding.

Can be overcome with increasing [] of ACh

Question 27

Depolarising block of succinylcholine

Answer 27

Succinylcholine isn’t quickly degraded

Succinylcholine opens the sodium ion channels and keeps them open

This maintains depolarisation- then sodium ion channels become inactivated- this fails to activate adjacent Na+ channels besides they gave become inactivated

Question 28

What is myasthenia gravis

Answer 28

An auto immune disease targeting nACh receptors making them nonfunctional

End plate potential are reduced in amplitude- no AP -leading to muscle weakness and fatigue

Question 29

Diagnosing myasthenia gravis

Answer 29

Edrophonium prevents ACh esterase from breaking down ACh so it build up in the synaptic cleft

This allows the weakness to be overcome by the increase in amplitude of the endplate potential as there is enough ACh to bind to as many functional nACHr as possible

Question 30

Organophosphate poisoning

Answer 30

Acetylcholinesterase inhibitors that form a stable irreversible covalent bond to the enzyme

• Recovery from poisoning may take weeks as synthesis of new acetylcholinesterase enzymes is needed

Question 31

What is the difference between nACHR and mACHhR

Answer 31

Nicotinic produce a fast depolarisation because it is a ligand gated ion channel

Muscuranic produce a slower response because they are coupled to G-proteins which trigger a cascade of events in the cell

Question 32

what properties of the myelin sheath allow saltatory conduction to occur?

Answer 32

high resistance

low electrical capacity