Sesh 5: Action Potential And The NMJ

Question 1

Depolarisation to threshold initiates an action potential at what part of the axon?

Answer 1

The axon hillock.

Question 2

Why does the Na+ current diminish if the voltage is held at +20mV during a voltage clamp experiment?

Answer 2

Voltage-gated Na+ channels inactivate

Question 3

Why does the action potential have an ‘undershoot’ phase?

Answer 3

Voltage-gated K+ channels don’t inactivate, therefore don’t close immediately when resting potential is reached, meaning they still drive the m.p. Towards Ek, resulting in hyperpolarisation.

Question 4

What happens during the absolute refractory period?

Answer 4

Voltage-gated Na+ channels are inactivated due to blockage of their pore via their inactivation particle.

Question 5

What is the relative refractory period?

Answer 5

Occurs for about 4ms after the absolute refractory period. Voltage-gated Na+ channels are now closed and recovering from inactivation. A strong stimulus may cause them to open and initiate an action potential.

Question 6

What makes up the functional part of voltage-gated Na+ channels?

Answer 6

An alpha subunit with 4 homologous repeats- each with 6 transmembrane domains.

Question 7

What has to occur for the inactivation particle to unblock the voltage-gated Na+ channel pore?

Answer 7

Membrane hyperpolarisation.

Question 8

What does a voltage-gated K+ channel need to be functional, and how is this different from a voltage-gated Na+ channel?

Answer 8

Needs 4 alpha subunits together, whereas Na channel only needs 1 alpha subunit to be functional.

Question 9

How do local anaesthetics, such as procaine, work?

Answer 9

By blocking voltage-gated Na+ channels when they are in the open or inactivated state, thereby blocking the action potential in pain fibres.

Question 10

Which axon class has the highest conduction velocity, and where are these axons found?

Answer 10

• A alpha

- Motoneurones to skeletal muscle, and sensory fibres to muscle spindle

Question 11

A nerve fibre is composed of several ______.

Answer 11

Axons

Question 12

What is the local current theory?

Answer 12

Injection of current into an axon will cause an immediate local change in membrane potential due to Na+ influx. However, this local current dissipates.

Question 13

Is conduction velocity higher in smaller or larger diameter axons?

Answer 13

Larger.

Question 14

What is the length constant of an axon?

Answer 14

The distance along the axon it takes for the initial depolarisation to fall to 37% of its original value.

Question 15

What is capacitance?

Answer 15

The ability of a membrane to store charge. Lower capacitance= higher conduction velocity.

Question 16

What is membrane resistance determined by?

Answer 16

The number of open ion channels in the membrane. High resistance= few ion channels open= greater conduction velocity.

Question 17

How does myelination change the membrane capacitance and resistance?

Answer 17

It insulates the axon, so lowers capacitance and increases resistance, to increase membrane conduction velocity.

Question 18

Why can the action potential only travel in one direction?

Answer 18

Because the region of axon behind the action potential is refractory- v-gated Na channels are inactivated

Question 19

In a myelinated neurone, how is conduction velocity related to fibre diameter?

Answer 19

Linearly

Question 20

In unmyelinated neurones, how is conduction velocity related to fibre diameter?

Answer 20

Conduction velocity is proportional to the square root of fibre diameter.

Question 21

What is the most common demyelinating disease of the CNS?

Answer 21

Multiple Sclerosis

Question 22

How can a stronger stimulus be encoded?

Answer 22

Increased action potential frequency

Question 23

What type of calcium channels do dihydropyridines e.g. Nifedipine block?

Answer 23

L-type

Question 24

Compared to voltage-gated Na+ channels, do voltage-gated Ca2+ channels activate/ inactivate more slowly or quickly?

Answer 24

More slowly.

Question 25

If extracellular Ca2+ is reduced, what will happen to the motor end plate potential?

Answer 25

The amplitude will be reduced.

Question 26

How is the action potential at the neuromuscular junction terminated?

Answer 26

AChesterase degrades ACh in the cleft.

Question 27

What is tubocurarine, and how does it work?

Answer 27

A neuromuscular blocker that works by blocking nicotinic ACh receptors, via binding to the ACh binding site.
A competitive nAChR blocker.

Question 28

What is succinylcholine, and how does it work?

Answer 28

A neuromuscular blocker that blocks nicotinic ACh receptors.
Acts as a depolarising blocker, by binding to ACh receptors, and prolonging depolarisation, thereby inactivating adjacent Na+ channels.

Question 29

What is Myasthenia Gravis?

Answer 29

An autoimmune disease of which sufferers produce auto-antibodies to nicotinic ACh receptors on skeletal muscle.
NAChRs are then degraded, reducing motor endplate potentials, leading to muscle weakness and fatigue.

Question 30

What are muscarinic AChR’s and where are they found?

Answer 30

GPCR’s that bind ACh on target tissue innervated by the parasympathetic NS.