Lecture 9 - Action Potentials

Question 1

What is an action potential?

Answer 1

The rapid depolarisation followed by repolarisation in a characteristic pattern

Question 2

What does an action potential depend on to cause the changes in potential difference?

Answer 2

Ionic gradients + selective permeability of the membrane to ions

Question 3

What needs to be reached in order for an action potential to be fired?

Answer 3

Threshold potential

Question 4

Why is an action potential described as being all or nothing?

Answer 4

If threshold potential is not reached then NO action potential

If threshold potential is reached there will always be an action potential that reaches the set membrane potential

Question 5

What is meant by action potentials are propagated without loss of amplitude?

Answer 5

They do not lose their height/maximum point of depolarisation

Height of the depolarisation stays the same

Question 6

What are the 5 properties of an action potential?

Answer 6

Rapid change in voltage across a membrane
Depends on ionic gradients and the selective permeability of the membrane to ions
Only happens if threshold level reached
All or nothing
Propagated without loss of amplitude

Question 7

How does the length of action potentials in the heart/SAN compare to axons and skeletal muscle?

Answer 7

Skeletal muscle = short (0.5ms)

SAN/Cardiac ventricle = LONGER (100ms)

Question 8

How does membrane selectivity (conductance) for an ion affect the membrane potential for the cell?

Answer 8

Higher the membrane selectivity/conductance for that ion the closer the membrane potential gets to the Equilibrium potential for that ion (Eion)

Question 9

What effects membrane selectivity/conductance to an ion?

Answer 9

Number of the ion channels open to that ion

Question 10

What causes the rapid upstroke in an action potential?

Permeability/conduction to what ion increases?
Which direction do these ions move and why?
What ion channel is affected?

Answer 10

Na+
Na+ influx down its electrochemical gradient
Voltage gated sodium channels (VGSC)

Question 11

How can the upstroke of action potential be referred to as an example of positive feedback?

Answer 11

Once threshold potential is reached from the influx of Na+ ions, more and more Na+ voltage gated ion channels (VGSC) open allowing influx of more and more Na+

Question 12

When do the voltage gated sodium ion channels inactivate?

Answer 12

The peak of the depolarisation

Question 13

When do the Potassium voltage gated ion channels open in an action potential?

Answer 13

Following the inactivation of the Na+ voltage gated ion channels at the peak of depolarisation

Question 14

In the action potential why is the Na+/K+ ATPase NOT involved in the repolarisation of the action potential?

Answer 14

It is working all the time trying to maintain the gradient of Na+ and K+

Question 15

What are the 2 stages to recovery after an action potential?

Answer 15

ARP = Absolute refractory period

RRP = Relative refractory period

Question 16

What is important about the Absolute Refractory Period and why does this happen?

Answer 16

Another action potential can not be propagated in this period
All/most Na+ Voltage gated ion channels are INACTIVATED

Question 17

What is the Relative Refractory period (RRP)?

Answer 17

Starts hen VGSC no longer inactivated
VGSC recovering from inactivation
Number of VGSC in inactivated state decreases as they become closed

Question 18

What is different about the Absolute refractory period compared to the relative refractory period?

Answer 18

ARP an action potential can never be propagated

RRP it is possible for another AP its just difficult

Question 19

What are the 3 states a voltage gated sodium ion channel can be in?

Answer 19

Closed
Open
Inactivated

Question 20

What is the difference of a VGSC being closed or inactivated?

Answer 20

When closed, depolarisation causes it to open

When inactivated, no amount of depolarisation will cause it to open

Question 21

What changes a VGSC from inactivated to closed?

Answer 21

Hyperpolarisation

Question 22

How many subunits make up a voltage gated Na+ channel?

Answer 22

4

Question 23

What is the significance of charged amino acids being present on the repeats I and IV of a VGSC?

Answer 23

Found in the membrane space
They react to changes in membrane potential causing the conformational change opening or closing the channel

Question 24

What is the inactivation particle of a VGSC?

Answer 24

Structure that blocks the pore of the VGSC inactivating it

Question 25

What 2 repeat units of the VGSC does the inactivation particle connect between?

Answer 25

III and IV

Question 26

How many alpha subunits make up a VGSC?

Answer 26

1

Question 27

How does the size of a Voltage Gated Potassium channel relate to a VGSC?

Answer 27

VGPC SMALLER than VGSC

Question 27

How does the size of a Voltage Gated Potassium channel relate to a VGSC?

Answer 27

VGPC SMALLER than VGSC

Question 28

What is a significant difference in the structure of a voltage gated potassium channel compared to a VGSC?

Answer 28

VGSC have an INACTIVATING PARTICLE so can be INACTIVATED VGPC do NOT have an inactivating particle

Question 29

What is the significance of the VGPC not having an inactivating particle?

Answer 29

They slowly close which is what causes the excess efflux/trickling of K+ out of the cell causing HYPERPOLARISATION

Question 30

How many alpha subunits make up a VGPC?

Answer 30

4

Question 31

What is an anaesthetic?

Answer 31

Drug which causes numbness/inability to feel pain (analgesia)

Question 32

What is Lidocaine?

Answer 32

Anaesthetic

Question 33

What are they 2 forms of local anaesthetics?

Answer 33

Protonated Unprotonated

Question 34

Which form of local anaesthetic is membrane soluble?

Answer 34

Unprotonated/uncharged

Question 35

What channels do local anaesthetics block?

Answer 35

Na+ channels

Question 36

Which form of the local anaesthetic enters the membrane and then which form causes the block affect?

Answer 36

Uncharged/Unprotonated enters the membrane Charged/protonated form causes the block

Question 37

What are the 2 blocking pathways of the Na+ that local anaesthetics act by?

Answer 37

Hydrophilic pathway Hydrophobic pathway

Question 38

What is the hydrophilic pathway of local anaesthetic block?

Answer 38

Blocks open channel/pore (Prevents Na+ moving in)

Question 39

What is the hydrophobic pathway of anaesthetic block?

Answer 39

Blocks pore of inactivated Na+ channel (Prevents reactivation)

Question 40

Why is important that VGSC get inactivated in the Absolute Refractory Period?

Answer 40

Prevents excess influx of Na+ preventing cell becoming to depolarised and therefore slowing down action potentials due to repolarisation being slower Ensures unidirectional propagation of action potentials

Question 41

How does diameter of an axon relate to conduction velocity?

Answer 41

Larger diameter = Faster Conduction velocity

Question 42

What is local current theory?

Answer 42

If a current/action potential is injected into an axon, the resulting charge/depolarisation will spread/diffuse along the axon causing an immediate local change

Question 43

What is Length constant (λ)?

Answer 43

The distance taken for the membrane potential to fall to its original value

Question 44

How does length constant relate to speed of action potential conductance?

Answer 44

LARGER length constant = faster conductance velocity

Question 45

What is Capacitance?

Answer 45

The ability to store charge Its a property of the lipid bilayer (doesn’t change)

Question 46

What is the effect of a high capacitance?

Answer 46

Voltage changes more slowly in response to current injection

Question 47

What does membrane resistance depend on?

Answer 47

The number of ion channels open

Question 48

What does the spread of a local current depend on?

Answer 48

Membrane resistance Capacitance

Question 49

How does a lower resistance effect length constant?

Answer 49

Longer/larger length constant

Question 50

What happens when local depolarisation/local current injected into an axon spreads down the axon?

Answer 50

If depolarisation reaches threshold, AP propagated

Question 51

What is important about the refractory period?

Answer 51

Ensures unilateral propagation of action potentials

Question 52

What cells myelinate axons of the PNS?

Answer 52

Schwann cells

Question 53

What cells myelinate axons of the CNS?

Answer 53

Oligodendrocyte

Question 54

What are the regions along a myelinated axon called that have no myelination called?

Answer 54

Nodes of Ranvier

Question 55

What is resistance and capacitance like under the myelinated region of a myelinated neurone compared to the nodes of Ranvier?

Answer 55

Higher Resistance Decreased capacitance

Question 56

How does myelination increase conduction velocity?

Answer 56

Inc membrane resistance Dec membrane capacitance Both cause INC in length constant

Question 57

What is saltatory conduction?

Answer 57

Reduced capacitance under myelin sheath means the local current spreads further down the axon to delpolarise the next node without firing an AP under the myelin sheath area The way the action potential quickly jumps from node to node in a myelinated axon Length constant is increase so local circuit current depolarise the next node above threshold

Question 58

What is Multiple sclerosis?

Answer 58

Myelin sheath of all CNS nerves attacked

Question 59

What is Devic’s disease?

Answer 59

Optic and spinal cord nerves demyelinated

Question 60

What nerves are demyelinated in Landry-Guillain-Barre syndrome and Charcot-Marie-Tooth disease?

Answer 60

PNS nerves

Question 61

Why does demyelination of axons cause problems?

Answer 61

Local current May not be able to spread enough to cause depolarisation to reach threshold at the next node of Ranvier