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Semester 1 - ICPP > Electrical Excitability > Flashcards

Electrical Excitability Flashcards

1
Q

What is an action potential?

A

Change in voltage across membrane

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2
Q

What do action potentials depend on?

A
  • Depends on ionic gradients and relative permeability of the membrane
  • Only occurs if a threshold level is reached
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3
Q

Where in the axon is an action potential generated?

A

Axon hillock

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4
Q

Describe how Depolarization to threshold initiates an action potential at the axon hillock

A

An action potential arriving at a synapse cause the release of neurotransmitters high cause depolarisation. The depolarisation has to spread across the dendrite to the axon hillock and depolarise it beyond the threshold to induce an action potential.

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5
Q

What happens if the conductance or permeability to any ion is increased in a membrane?

A

the membrane
potential (Vm) will move closer to the equilibrium potential for that
ion.

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6
Q

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

A

the number of channels for the ion that are open.

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7
Q

How many ions are needed to move to produce a relatively large
change in the membrane potential?

A

Very small amount

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8
Q

What are the 4 stages of an action potential?

A
  1. Depolarisation
  2. Repolarisation
  3. Hyperpolarisation
  4. Refractory period
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9
Q

What happens during the depolarisation period of an action potential?

A

The arrival of an action potential causes depolarisation which causes sodium ion channels to open. The influx of sodium ions cause further depolarisation. The membrane potential increases until the sodium ion channels become inactivated.

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10
Q

What happens during repolarisation?

A

Inactivation of sodium ion channels as well as opening of potassium ion channels resulting in efflux of potassium ions results in the membrane potential decreasing.

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11
Q

Why does hyperpolarisation occur?

A

The membrane potential decreases below the resting potential because more potassium channels open than sodium channels and they close more slowly resulting in more potassium ions leaving than sodium ions that entered

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12
Q

What is happening during the absolute refractory period?

A

nearly all Na+ channels are in the inactivated state

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13
Q

What are the advantages of the absolute refractory period?

A

The absolute refractory period limits the rate of firing of action potentials. It also prevents action potentials from traveling backward along the axon, because the region of the axon that has just produced the action potential is “refractory.”

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14
Q

What is happening during the relative refractory period?

A

Na+ channels are recovering from inactivation, the excitability returns towards normal as the number of Na+ channels in the inactivated state decreases and as the number of open voltage-gated K+ channels close. An action potential will be generated if a stronger than normal stimulus is applied.

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15
Q

Describe the structure of voltage-gated Na+ channel

A

• Functional Na+ channel only one α subunit.
• One α subunit consists of four
similar sections(quarters)or repeats.
• The 4 quarters join to make a pore in the middle which allows sodium ions through but excludes any other ions.
• Between quarter 3 and 4 there is an inactivation particle in the intracellular membrane which is what goes into the pore and block the pore to stop movement of ions

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16
Q

How is the conformation change in voltage gated sodium channels brought about?

A
  • Each quarter has some membrane spanning domains.
  • The S4 domain has positively charged amino acids residing within the membrane. The positive charges are sitting in a voltage field.
  • If you change voltage field , the charged amino acids will have a different charge on them- this is what causes the conformational change in the ion channel to cause it to open .
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17
Q

How is the structure of voltage-gated K+ channels different to voltage-gated Na+ channels?

A
  1. voltage-gated Na+ channels have one α subunit that is split into four sections whereas voltage-gated K+ channels have four individual α subunits
  2. voltage-gated Na+ channels have an inactivation particle which inactivated the channel but voltage-gated K+ channels do not have one
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18
Q

How is the structure of voltage-gated K+ channels similar to voltage-gated Na+ channels?

A
  1. They both have a membrane spanning domain with positively charged amino acid that can detect changes in voltage field and cause conformational change in the protein and cause the pore to open.
  2. They both have a pore region which contributes to selectivity
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19
Q

How do local anaesthetics work?

A

Local anaesthetics block Na+ channels so that reduced influx of sodium ions so less depolarisation so prevents action potentials being fired. blocking action potentials in pain sensing fibres reduces pain

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20
Q

What is the order in which anaesthetics block axons?

A
  1. small myelinated axons 2. un-myelinated axons

3. large myelinated axons

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21
Q

What is the difference between protonated and non protonated forms of local anaesthetics?

A

the unprotonated form is membrane permeable. The protonated form is membrane impermeable

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22
Q

How is the action potential conducted along an axon?

A

• A change in membrane potential in one part can spread to adjacent areas of the axon
• This occurs because of local current spread
• Conduction velocity is determined by how far along
the axon these local currents can spread
• When local current spread causes depolarization of part of
the axon to threshold then an action potential is initiated in
that location

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23
Q

What does Spread of local current depend on?

A

membrane resistance and capacitance

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24
Q

What are the factors that affect conduction velocity?

A
  • Diameter of axon - large diameter conducts more quickly- small diameter axons conduct more slowly
  • Meylination
25
Q

What does injection of current into an axon cause?

A

Injection of current into an axon will cause the resulting charge to spread along the axon and cause an immediate local change in the membrane potential.

26
Q

What is capacitance?

A

The ability to store charge

27
Q

What does the membrane resistance depend on?

A

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

28
Q

What does high capacitance mean for the voltage?

A

voltage changes more slowly in response to current injection

29
Q

What does high resistance mean fro the voltage?

A

change in voltage spreads further along the axon

30
Q

What increases the spread of local change in the membrane potential?

A

high membrane resistance and low membrane capacitance – the longer this distance
the faster the conduction

31
Q

Why is it important that Na+ channels become inactivated?

A

To stop the positive feedback loop and maintain the directionality of the action potential.

32
Q

What is the consequence of the delayed closing o voltage gated K+ channels?

A

Allows hyperpolarisation to occur which Increases rate of recovery of certain channels form inactivation

33
Q

How does myelination improve conduction?

A
  • large increase in membrane resistance (Rm)
  • large decrease in membrane capacitance (Cm)
  • these increase length constant (λ)
  • slight decrease in time constant (τm)

conduction velocity ∝ λ / τm

34
Q

What is the length Constance?

A

The distance it takes for the potential to fall to 37% of its original value

35
Q

List 4 diseases that result from breakdown or damage the myelin sheath?

A

Central Nervous System
• Multiple sclerosis – all CNS nerves
• Devic’s disease – optic and spinal cord nerves only

Peripheral Nervous System
• Landry-Guillain-Barre syndrome
• Charcot-Marie-Tooth disease

36
Q

In regions of demyelination, why is the density of the action current reduced?

A

because of resistive and capacitive shunting.

37
Q

Summarise the Generation of the action potential

A

• depolarization to threshold triggers the opening of many voltage gated Na+ channels
• the influx of Na+ produces the rapid upstroke of the action potential (membrane potential moves towards ENa)
• this depolarization causes inactivation of Na+ channels and opening of voltage- gated K+ channels
• Na+ influx stops and the increased K+ efflux leads to repolarization (membrane potential moves towards EK)
• relatively little ions move and the Na/K ATPase is NOT involved in action
potential repolarization

38
Q

Summarise conduction of the action potential

A

• an action potential causes local current flow leading to an immediate
depolarization of adjacent bits of the axon
• where this local depolarization reaches threshold an action potential is initiated

39
Q

What is Saltatory conduction?

A

The action potential “jumps” from node to node allowing a much faster conduction velocity. An action potential occurs only at the nodes.

40
Q

What is a neuromuscular junction?

A

The neuromuscular junction is the synapse between a nerve and a skeletal muscle fibre.

41
Q

What happens at the nerve terminal

A
  1. An action potential arrives causing voltage gated calcium channels to open
  2. Ca2+ entry through Ca2+ channels
  3. Ca2+ binds to synaptotagmin
  4. Vesicle brought close to membrane
  5. Vesicles fuse with a protein called Snare complex which make a fusion pore
  6. Transmitter released through this pore
42
Q

How does increasing the frequency of action potential affect the amount of nerve terminal calcium ion entry?

A

Increasing frequency of action potentials increases amount of nerve terminal Ca2+ entry

43
Q

Which ion channels are present in the nerve terminal?

A
  • voltage-gated Na+ channels
  • voltage-gated K+ channels
  • voltage-gated Ca2+ channels
44
Q

Describe the structure of calcium ion channels

A

The structure of the α-subunit of voltage-gated Ca2+ channels is very similar to voltage-gated Na+ channels. - made of 4 subunits

Have positively charged amino acids which will detect a change in membrane potential. Depolarisation will cause conformational change in channel which causes opening of pore and influx of calcium ions

45
Q

Describe the Subunit composition of Na+ and Ca2+ channels

A

A pore forming subunit is necessary for a functional channel.

Other associated subunits fine-tune the properties and enable correct regulation of channel activity

46
Q

List 3 properties of calcium channels when compared with sodium channels

A
  • Voltage-gated Ca2+ channels activate more slowly than voltage-gated Na+ channels
  • Ca2+ channels activate and inactivate – but much more slowly than Na+ channels
  • Ca2+ channel inactivation is Ca2+-dependent and voltage dependent
47
Q

Describe what happens after the release of neurotransmitter

A
  • The acetylcholine diffuse across the synaptic cleft and binds to the nicotinic acetycholine receptor causing a conformational change in the receptor which is equally permeable to sodium and potassium causing it to open.
  • Despite the ion channel being equally permeable to sodium and potassium, it opening causes depolarisation because the membrane potential is originally very negative, far away from the sodium equilibrium potential. So there is a big driving force for sodium entry. The overall effect of the channel opening is that the membrane potential will move towards the sodium equilibrium potential.
  • However, as the membrane potential rises, it gets further away from the potassium equilibrium potential, which causes potassium ions to leave. However the initial rise is enough to depolarise the skeletal muscle to threshold to generate an action potential called the end plate potential.
48
Q

What type of channel is a nicotinic acetylcholine receptor?

A

The nicotinic acetylcholine receptor (nAChR) is a ligand gated ion channel.

49
Q

How is transmitter release dependent on Ca2+ entry?

A

end plate potentials decrease in amplitude as external Ca2+ is lowered

50
Q

What are end plate potentials?

A

• End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction.

51
Q

Summarise the transmission at the neuromuscular junction

A

• Action potential arrives at the motoneurone terminal where it opens voltage-
gated Ca2+ channels.
• Ca2+ entry initiates exocytosis of vesicles containing ACh.
• ACh binds to nicotinic ACh receptors on the muscle end-plate, causes them
to open and the flow of cations causes a depolarization called the end-plate
potential.
• The end-plate potential depolarizes the adjacent muscle membrane and
activates voltage-gated Na+ channels, thereby initiating an action potential in
the muscle fibre which then contracts due to excitation-contraction coupling.

52
Q

What are the two types of Blockers of nicotinic ACh receptors?

A

competitive blocker depolarizing blocker

53
Q

Give an example of how a competitive blocker works

A

D-tubocurarine (d-TC) binds to the nicotinic acetylcholine receptor which does not cause a conformational change so no depolarisation. Therefore, released acteylcholine will not cause depolarisation as they cannot bind to the receptor. Therefore cannnot cause muscle contraction

54
Q

How do you overcome The block by d-TC?

A

by increasing the concentration of ACh

55
Q

Give an example of how depolarising blocker works?

A

succinylcholine Activate nicotinic acetylcholine receptors and maintain depolarisation as it is not broken down by acteylcholine esterase. This causes sodium ion channels to open initially but with time, sodium channels around neuromuscular junction become inactivated. Even if acetylcholine binds, it cannot cause depolarisation as it encounters the inactivated sodium channels. This blocks the transmission between the nerve and muscle

56
Q

What is Mayasthenia gravis?

A

an autoimmune disease targeting nACh receptors.

• Patients may suffer profound weakness
• Weakness increases with exercise
• Caused by antibodies directed against nAChR on postsynaptic membrane
of skeletal muscle
• Antibodies lead to loss of functional nAChR by complement mediated lysis
and receptor degredation
• Endplate potentials are reduced in amplitude leading to muscle weakness
and fatigue

57
Q

How is myasthenia gravis diagnosed?

A

The edrophonium test confirms myasthenia gravis. Facial weakness is provoked by repeated facial movements. Edrophonium chloride, a short-acting anticholinesterase, is then given by slow intravenous injection. In myasthenia gravis the facial weakness is relieved rapidly by this test

58
Q

How does Organophosphate poisoning work?

A

• 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

Semester 1 - ICPP (7 decks)

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