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ESA1 - Physiology and Pharmacology > Action Potential > Flashcards

Action Potential Flashcards

1
Q

What are some features of an action potential?

A

Change in voltage across membrane, depends on ionic gradients and permeability of the membrane, only occurs if threshold is reached, all or nothing principle, propagated without loss of amplitude

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2
Q

What initiates an action potential at the axon hillock?

A

Depolarisation to threshold

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3
Q

What happens to the membrane potential if the conductance (g) to any ion is increased?

A

Moves closer to the equilibrium potential for that ion

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4
Q

What is the conductance of the membrane to a particular ion dependent on?

A

Number of channels for that ion that are open

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5
Q

What is capacitance?

A

Ability to store charge

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6
Q

Each action potential increases [Na+] in the axon by how much?

A

40 micromoles. If the resting [Na+] is 10 micromoles this represents an increase of 0.4%

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7
Q

What do voltage clamps enable?

A

Membrane currents to be measured at a set membrane potential

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8
Q

What does the absolute refractory period mean?

A

No matter how strong the stimulus, you cannot initiate action potential

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9
Q

What does the relative refractory period mean?

A

If the stimulus is strong enough, you can produce an action potential

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10
Q

What state are nearly all Na+ channels in during the ARP?

A

Nearly all Na+ channels are in the inactivated state

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11
Q

What state are the Na+ channels in during the RRP?

A

Na+ channels are recovering from inactivation, the excitability returns towards normal as the number of channels in the inactivated state decreases

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12
Q

How many subunits in a voltage gated Na+ channel?

A

Na+ channel is one peptide subunit split into 4 parts

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13
Q

What is the significance of the pore of Na+ channels?

A

Voltage field that changes. Change in membrane potential will change voltage field and cause conformational change in the channel, pore will open. When pore is open, it is susceptible to inactivation as the inactivation particle can block the pore.

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14
Q

How many subunits are needed to make a functional potassium channel?

A

Four alpha subunits

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15
Q

What is the basic structure of voltage gated K+ channels?

A

S4 region has positive amino acid residues contributing to voltage sensitivity. P region contributes to pore selectivity.

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16
Q

How do local anaesthetics such as procaine act?

A

Mainly by blocking Na+ channels.

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17
Q

In which order do local anaesthetics block axons?

A
  1. Small myelinated axons
  2. Un-myelinated axons
  3. Large myelinated axons
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18
Q

What does a nerve fibre comprise of?

A

Several axons with different diameters

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19
Q

What does membrane resistance depend on?

A

Number of ion channels open - the lower the resistance, the more ion channels are open

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20
Q

What happens when capacitance is high?

A

Voltage changes more slowly in response to current injection

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21
Q

What happens when resistance is high?

A

Change in voltage spreads further along the axon

22
Q

What does myelination do to the spread of action potential?

A

Speeds it up as the action potential ‘jumps’ from node to node

23
Q

How does the myelin sheath improve conduction?

A
  1. Large increase in membrane resistance
  2. Large decrease in membrane capacitance
  3. Increase in length constant
  4. Slight decrease in time constant

(Conduction velocity proportional to length constant/time constant)

24
Q

What diseases result from breakdown or damage to the myelin sheath?

A

Multiple sclerosis (all CNS nerves)
Devic’s disease (optic and spinal cord nerves)
Laundry-Guillain-Barre syndrome (PNS)
Charcot-Marie-Tooth disease (PNS)

25
Q

How is signal passed form nerve to muscle?

A

Neuromuscular junction

26
Q

What ion channels are in the nerve terminal?

A

Voltage-gated Na+, K+ and Ca2+ channels

27
Q

In brief, what happens at the nerve terminal?

A

Depolarisation - opens voltage gated Ca2+ channels - Ca2+ entry - increase in intracellular concentration of Ca2+ - release of neurotransmitter

28
Q

Why can Ca2+ influx through Ca2+ channels raise the internal concentration of Ca2+ significantly?

A

Because the concentration of Ca2+ inside is so low

29
Q

What is Eca?

A

+122 mV

30
Q

What does increased frequency of action potentials increase at the nerve terminal?

A

Amount of Ca2+ entry - more transmitter released

31
Q

What is the structure of the alpha subunit of voltage-gated Ca2+ channels similar to?

A

Voltage gated Na+ channels

32
Q

Where are L-type Ca2+ channels primarily located?

A

Muscles, neurones, lung

33
Q

What are blockers of L-type calcium channels?

A

DHP (dihydropyridines) eg Nifedipine

34
Q

What is Nifedipine often used to treat?

A

Hypertension

35
Q

Do Ca2+ channels activate faster or more slowly than Na+ channels?

A

More slowly - they activate and inactivate but much more slowly than Na+ channels

36
Q

In recording of Ca2+ current in a snail neurone, what was shown?

A

When Ba2+ flows through the channels much less inactivation is seen thus increased intracellular concentration of Ca2+ leads to inactivation of Ca2+ channels

37
Q

What is Ca2+ inactivation dependent on?

A

Ca2+

38
Q

What breaks down acetylcholine?

A

Acetylcholine esterase

39
Q

How are transmitters released?

A
  1. Ca2+ entry through Ca2+ channels
  2. Ca2+ binds to synaptotagmin
  3. Vesicle brought cose to membrane
  4. Snare complex make a fusion pore
  5. Transmitter released through this pore
40
Q

What receptor channels does release of ACh activate?

A

Nictonic ACh receptor channels

41
Q

How many molecules of ACh are needed to cause a conformational change?

A

2

42
Q

When do end plate potentials decrease in amplitude?

A

As external Ca2+ is lowered

43
Q

What does the end-plate potential initiate?

A

Muscle action potential

44
Q

How does curare cause paralysis?

A

By blocking the transmission between nerve and muscle

45
Q

What is an example of a competitive blocker of nicotinic ACh receptors?

A

Tubocurarine

46
Q

What is an example of a depolarising blocker of nictonic ACh receptors?

A

Succinylcholine

47
Q

How can the block by tubocurarine be overcome?

A

Increasing concentration of ACh

48
Q

What is mayasthenia gravis?

A

An autoimmune disease targeting nACh receptors

49
Q

What is mayasthenia gravis caused by?

A

Antibodies directed against nAChR on postsynaptic membrane of skeletal muscle

50
Q

What is the difference in response between nicotinic and muscarinic ACh receptors?

A

nAChR produces a fast depolarisation because it is a ligand gated ion channel while mAChR produce a slower response as they are coupled to G proteins which trigger a cascade of events in the cell

ESA1 - Physiology and Pharmacology (11 decks)

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