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Human basic neuroscience > Action potentials > Flashcards

Action potentials Flashcards

1
Q

What had already been established in the early 20thc

A

Neurons respond to stimulation with ‘all-or-none’ spikes of electrical activity which self-propagate along axons

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2
Q

What did Bernstein propose as the cause of action potentials

A

Bernstein (1902)- due to transient loss of selective membrane permeability, which would lead to membrane potential to shoot to 0mV

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3
Q

Whydid the mechanisms underlying action potential generation remain obscure for a long time

A

It had not been possible to directly record the transmembrane potential in axons as they are so thin- electrophysiological studies on axons had relied on extracellular recordings

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4
Q

Who got a Nobel prize for the functions of neurons

A

1932- Sherrington and Adrian

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5
Q

Who got a Nobel prize for the function of single nerve fibres

A

1944- Erlanger and Gasser

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6
Q

Who got a Nobel prize for the mechanisms of axonal excitability

A

1963- Hodgkin and Huxley

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7
Q

Who got a Nobel prize for the study of single ion channels

A

1991- Neher and Sakmann

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8
Q

How were the first intracelllular recordings of the action potential carried out

A

Hodgkin and Huxley (1945)-used the giant axon of a squid as it is big enough to enable the insertion of microelectrodes into the axoplasm

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9
Q

What did the first intracellular recordings of action potential reveal

A

Hodgkin and Huxley (1945)- the membrane potential reversed during action potentials (overshot 0mV) then became transiently hyperpolarised below resting membrane potential following the action potential (after-hyperpolarisation)

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10
Q

What did the first intracellular recordings of action potential reveal about their cause

A

Hodgkin and Huxley (1945)- Could not be explanied by loss of selective membrane permeability, but rather changes in the permeability to specific ions

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11
Q

What is the sodium hypothesis

A

Suggested the upstroke of action potential could be explained by increased Na+ permeability- this could cause Na+ to diffuse into the cell, dragging the membrane potential towards the positive Nernst potential for Na+ ions (around 55mV)

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12
Q

Study investigating the sodium hypothesis

A

Nastuk and Hodgkin (1950)- plotting action potential peak against the log of extracellular Na+ conc reveals a straight line with a slope predicted by Nernst for Na+, though the membrane potential never quite reaches E Na due to leak channels

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13
Q

What increases the membrane permeability to Na+ in the action potential

A

Voltage-gated Na+ ion channels- if the membrane is depolarised the channels open and Na+ permeability increases, which increases membrane depolarisation, which increases Na+ permeability in a positive feedback loop

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14
Q

What 3 membrane conductances can be multiple phases of the action potential be explained by

A

Leak conductance, voltage-dependent Na+ conductance, voltage-dependent K+ conductance that all try to clamp the membrane potential at their Nernst potential

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15
Q

Which of the 3 membrae conductances determines the resting membrae potential

A

The leak conductance

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16
Q

Which of the 3 membrane conductances is recruited whe the membrane is depolarised

A

Voltage-dependent Na+ conductance- the membrane potential shoots towards E Na as the Na+ conductance increases in a positive feedback loop, dominating leak conductance

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17
Q

What happens to the Na+ conductance when the peak of the action potential is reached

A

Na+ conductance inactivates, and there is a delayed recruitement of voltage-dependent K+ conductance that drags the membrane potetial towards E K and rapidly repolarises the membrane

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18
Q

Which of the 3 membrane conductances causes the undershoot/after-hyperpolarisation

A

The K+ conductance takes time to turn off after repolarisation, causing the undershoot as the membrane is more permeable to K+ ions than at rest
When the K+ conductance turns off, the membrane potential is again set by leak conductance

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19
Q

What is it necessary to do in order to determine the properties of the ionic conductances underlying the action potential by manipulating membrane potential

A

Membrane potential affects membrane permeability which in turn affects membrane potential, so it is necessary to break this feedback loop in experiments

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20
Q

How can the membrane potential/permeability feedback loop be broken

A

Axial voltage-clamp- a wire is inserted along the length of an axon and connected to an electronic feedback circuit to clamp the axon’s membrane potential and prevent further depolarisation, while recording the current required to achieve this voltage clamp (Hodgkin and Huxley, 1952)

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21
Q

What does the axial voltage clamp allow the measurement of

A

Measurement of membrane currents as a function of time at any given voltage (Hodgkin and Huxley, 1952)

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22
Q

Hodgkin and Huxley (1952)- what was the effect of stepping the membrane potential to a depolarised level (0mV)

A

Reveals a transient inward current of Na+, followed by a sustained outward current of K+

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23
Q

Hodgkin and Huxley (1952)- how could the current for each ion be independently measured WITHOUT using pharmacological blockers

A

Removing Na+ from the extracellular fluid eliminates the inward current, leaving the delayed and sustained outward current mediated by the voltage-dependent K+ conductance.. subtraction can calculate the current mediated by the Na+ conductance

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24
Q

Hodgkin and Huxley (1952)- how could the current for each ion be independently measured using pharmacological blockers

A

Tetrodotoxin (TTX) blocks the Na+ conductance, while tetraethylammonium ions (TEA+) block the delayed K+ conductance

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25
Q

Hodgkin and Huxley (1952)- what is the effect of increasingly large voltage steps on K+ conductance

A

K+ current is larger and faster to activate with increasingly large depolarisation steps due to an increase in K+ conductance and an increase in driving force- once fully activated, the K+ conductance is sustained throughout the voltage step

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26
Q

Hodgkin and Huxley (1952)- how can conductance be calculated from the current over time

A

Ohm’s law can be used to calculate conductance

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27
Q

Hodgkin and Huxley (1952)- what is the effect in Na+ conductance of a a given voltage step compared to the effect on K+ conductance

A

Na+ conductance activates more quickly than K+ conductance, and the rate of activatino increases with depolarisation

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28
Q

Hodgkin and Huxley (1952)- what is the size of the effect of voltage increase on Na+ conductance

A

Na+ conductance increases monotonically as a function of voltage

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29
Q

Hodgkin and Huxley (1952)- what happens to Na+ current as the membrane potential approaches the Nernst potential for Na+

A

Na+ current decreases due to the decrease in driving force

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30
Q

Hodgkin and Huxley (1952)- what is the effect on Na+ of voltage steps above Na+’s Nernst potential

A

Na+ current reverses, and Na+ ions are driven out of the cell (situation would not happen during an action potential))

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31
Q

Hodgkin and Huxley (1952)- what happens to Na+ conductance followig activation

A

It shows rapid inactivation, even if the membrane remains depolarised
The rate of inactivation increases with depolarisation

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32
Q

What is subthreshold Na+ conductance

A

Weak inputs may be sufficient to active voltage-gated Na+ conductances, without evoking an action potential

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33
Q

How can weak inputs activate voltage-gated Na+ conductances without evoking an action potential

A

The increases in the K+ leak current (due to increased driving force from depolarisation) and voltage-gated K+ current can counterbalance the depolarising Na+ current, preventing entry into the positive feedback loop

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34
Q

What does action potential threshold reflect

A

A point at which the outward currents can no longer counterbalance the inward currents- not an intrinsic property of the Na+ conductance, but dynamic

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35
Q

What happens if voltage-gated K+ conductance is blocked during an action potential

A

The membrane can still repolarise, as the Na+ conductance deactivates, just more slowly

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36
Q

What is the role of the voltage-gated K+ conductance

A

Speeding up repolarisation enabling the axon to fire again with a shorter delay, maximal firing rate

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37
Q

Why does the refractory period occur

A

It takes time for the Na+ conductance to de-inactivate, and for the voltage-gated K+ conductance to de-activate- in this time, the membrane is hypoexcitable

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38
Q

What is the absolute refractory period

A

The time where it is impossible to evoke another action potential no matter how large the stimulus, because the fraction of Na+ conductance available for activation is not sufficient to overcome the leak/K+ conductance

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39
Q

What is the relative refractory period

A

The time when a higher threshold is required for another action potential to be fired, as only a limited proportion of the Na+ conductance has recovered from inactivation and voltage-gated K+ conductance has not been fully deactivated

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40
Q

What technique allows us to record the activity of single ion channels

A

Patch-clamp techniques

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41
Q

What is the behaviour of single voltage-dependent ion channels following the onset of a voltage step

A

The current flowing through single channels flips ‘on’ and ‘off’ in a stochastic manner, with the currents looking different from trial to trial- it does not show a smooth increase

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42
Q

What do the macroscopic currents recorded by Hodgkin and Huxley represent

A

The statistical behaviour of a large no of channels, which shows stereotypical patterns from trial to trial

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43
Q

How do neurons encode information

A

In the rate and/or timing of action potentials

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44
Q

Why is fast conductance important for behaviour

A

For the CNS to function, signals must be conducted from the periphery, processed, and transmitted back to effector organs over behaviourally relevant timescles (eg sufficient to catch a prey, remove a hand from a hot plate before tissue damage)

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45
Q

What range does the speed of action potential conduction vary over

A

<1ms/s to over 100m/s

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46
Q

What physical properties of axonal fibres affect their conductance velocity

A

Diameter and myelination

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47
Q

Study showing that conduction velocity is not a hard-wired property of an axon

A

There is continued remodelling of myelination throughout life and learning can induce white matter plasticity (Scholz et al, 2009)

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48
Q

Why will changes in conductance velocity alter the synchronisation across multiple inputs

A

The inputs arriving onto neurons have to travel over a variety of distances so will experience different conduction delays
Changes in conduction velocity will thus alter synchronisation and modulate how info is processed

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49
Q

What may axonal plasticity be an importatnt process during

A

Brain development and learning

50
Q

How dos membrane capacitance affect the response of the membrane

A

It slows it down, as it takes time to charge up the membrane to its new value

51
Q

What is the speed of response of the membrance characterised by

A

Time constant T- the amount of time it takes for the change in potential to reach 63% of its final value

52
Q

What is the effect of capacitance and membrane resistance on the time constant

A

The lower the capacitance and membrane resistance, the shorter the time constant aka the faster the membrane responds to a stimulus

53
Q

What is the equation for the time constant

A

Tau = 𝒓𝒎*𝑪𝒎

rm is membrane resistance, Cm is membrane capacitance

54
Q

What happens to the speed of response as the signal propagates along the cable

A

The membrane is leaky, so as the current gradually leaks across the membrane the response decays exponentially

55
Q

What is the length constant

A

The distance along a cable over which the steady-state signal decays to 37% of its original value

56
Q

What is the equation for length constant

A

(𝝀 =+√(rm/ri ))

rm and ri are membrane and internal resistances

57
Q

What is the effect of membrane and and internal resistance on length constant

A

The higher the membrane resistace and the lower the internal resistance, the longer the signal can travel without decaying as much (higher length constant)

58
Q

What happens to the current flowing across the membrane as the membrane charges up

A

It will decrease, thus the current flowing down the axon will increase correspondingly

59
Q

What is λ for cortical axons

A

A few hundred microns

60
Q

How does the action potential curve map onto an action potential moving along an axon length

A

The sharp peak is at the point at which the action potential is being actively generated, with a leading edge of subthreshold depolarisation and a wake of refractory axon showing Na+ channel inactivation/after-hyperpolarisation

61
Q

What does the refractory wake of the action potential curve ensure

A

Ensures that the action potential only propagates in one direction

62
Q

What does conduction velocity relate to in terms of the axon

A

How fast the active site of generation moves along the axon, aka how quickly the next segment of axon can be depolarised to threshold

63
Q

How does conduction velocity relate to length constant

A

Conduction velocity is proportionate to length constant

64
Q

How does conduction velocity relate to time constant

A

Conduction velocity is proportional to 1/tau

65
Q

Why do large diameter fibres have faster conductio velocities

A

Less internal resistance due to greater space for current to travel among organelles, decreased capacitance

66
Q

How does increasing axon diameter affect membrane capacitance

A

Increased membrane diamater increases membrane area which increases linearly with membrane capacitance as there is more capacitive membrane to charge up

67
Q

How does increasing diameter affect membrane resistance

A

Increased diameter means higher membrane area which means more channels, so decreased membrane resistance

68
Q

How does increasing diameter affect internal resistance

A

The square of the diameter is proportional to decreased internal resistance

69
Q

Formula showing the relationship between length constant and d

A

λ is proportional to√𝑑

70
Q

Why is time constant independent of diameter

A

Increased diameter increases membrane capacitance (increases time constant) but decreases membrane resistance (decreases time constant), so the 2 cancel each other out

71
Q

Considering the effect of diameter on time and length constant, how does diameter affect conduction velocity

A

Conduction velocity increases according to √𝑑, so an 100 fold increase in axon diameter will yield a 10 fold increase in conduction velocity

72
Q

How does myelination help enable high conduction velocities in relatively small diameter fibres

A

Oligodendrocytes/Schwann cells provide insulating sheaths around axons to enhance the passive propagation of electrical signals

73
Q

How does myelination affect membrane resistace

A

Membrane resistance increases in proportion to thickness of the myelin sheath, meaning less leakage of current of current across the membrane and faster passive propagation

74
Q

How does myelination affect membrane capacitance

A

Membrane capacitance decreases in proportion to thickness of the myelin sheath as increased space between the 2 conducting solutions either side of the membrane decreases the capacitance

75
Q

How does myelination affect the length and time constant

A

The length constant is increase proportional to √m, while tau is unaffected

76
Q

Why are the Nodes of Ranvier necessary

A

Myelin is not a perfect insulator, so as the signal propagates passively along the axon it decays- the Nodes of Ranvier are necessary to regenerate the action potential

77
Q

What are the Nodes of Ranvier

A

Regular interruptions of the myelin sheath, contain high densities of voltage-gated Na+ channels to regenerate the action potential

78
Q

What term describes the way the action potential jumps from node to ndoe

A

Salutatory conduction

79
Q

How does the amount of nodal membrane (length and membrane) affect rate of conduction

A

The greater the amount of nodal membrane (length and number) the slower conduction will be, as propagation in the ndoel region operates the same way as in unmyelinated axons

80
Q

What enables longer internodal regions (and fewer nodes) to increase salutaotry conduction speed

A

Higher velocity of passive conductance aka increased length constant

81
Q

What effect will increased total axon diameter of a myelinated axon have on myelin thickness

A

Increased axon AND myelin sheath thickness (as there is a fixed ratio between axon diameter and that of the total nerve)

82
Q

What is the effect of increased diameter increasing both axon and myelin thickness

A

Conductino velocity increases approximately linearly with total nerve diameter, as increased axon diameter and increased myelination both boost velocity

83
Q

What would be the effect of stripping away the segments of myelin sheath

A

Would leave a bare section of axon with low expression of voltage-gated Na+ channels- conduction can still occur even if 2-3 myelin segments are removed, but increased conduction delay eventually causes current to be shunted by the exposed membrane, causing conduction failure

84
Q

What is the difference in channels between demyelinated axons and unmyelinated axons

A

Unmyelinated axons have high densities of voltage-gated Na+ channels along their length (are meant to be unmyelinated)

85
Q

Examples of unmyelinated fibres

A

Slow conduction fibres, C fibres in periphery, local projections within grey matter

86
Q

What are unmyelinated fibres more efficient for and why

A

Myelination costs space and energy, so unmyelinated fibres are more efficient for signals that don’t need to be propagated quickly

87
Q

What diamater of unmyelinated axons are likely to conduct faster than myelinated fibres

A

Total diameters below 1um, as myelin takes up space

88
Q

What is an action potential

A

An all or nothing signal that conveys information by its rate and duration of firing over distances in the nervous system

89
Q

What does it mean that action potentials are all or nothing

A

They can only be generated if the cell becomes depolarised enough to reach the threshold, and always follow the same shape/duration/reaches the same peak voltage’sa

90
Q

What is an osscilloscope

A

A special type of voltmeter that can be used to study action potentials by recording the voltage across the membrane as it changes over time

91
Q

What identifiable parts does each action potential have

A

Threshold, rising phase where membrane is depolarised, overshoot, falling phase where rapidly repolarisation occurs, then the undershoot/after-hyperpolarisation, then a gradual restoration of the resting potential

92
Q

How long do action potentials last

A

Around 2msec

93
Q

How is the action potential triggered

A

Na+ voltage-gated sodium channels open at the axon hillock in response to a stimulus eg membrane stretching or the binding of neurotransmitters

94
Q

How do we generate multiple successive action potentials

A

Passing continuous current into a neuron with a microeelctrode

95
Q

What does the rate of action potential generation depend on (current)

A

The magnitude of the continuous depolarising current- if threshold is just reached the cell may generate 1 action potential per second (1Hz), but if current is increased the rate may increase to 50Hz

96
Q

How can stimulation intensity be encoding by action potential firing

A

A higher depolarising current means a higher rate of action potential firing

97
Q

What is the maximum firing frequency for a neuron and why

A

About 1000Hz, as the absolute refractory period is about 1msec

98
Q

How are the voltage-gated Na+ channels selective for Na+

A

They have pore loops assembeld into a selectivity filter, making the channel 12x more permeable to Na+ than K+

99
Q

What mechanism underlies the voltage-gating of the Na+ channel

A

A voltage sensor in segment s4 of the molecule that contains +ve amino acid residues regularly spaced along the helix coils, meaning the entire S4 coil can be twisted by a change in membrane potential, opening the gate

100
Q

What is the threshold for neurons

A

-40mV

101
Q

How long do the Na+ channels stay open for following threshold

A

Stay open for 1msec then inactivate when the membrane is depolarised

102
Q

Disorder demonstrating the importance of the Na+ channels closing quickly

A

Single amino acid mutations in the extracellular region of one sodium channel cause generalised epilepsy with febrile seizures which involves explosive electrical activity in the brain- the mutation slows the inactivation of Na+ channels, prolonging the action potential

103
Q

What is a channelopathy

A

A human genetic disease caused by alterations in the structure and function of ion channels

104
Q

Effect of TTX on voltage-gated sodium chael

A

Tetrodotoxin is a pufferfish toxin that is fatal if ingested- binds tightly to a site outside the channel blocking the pore and blocking all sodium-dependent action potentials

105
Q

Effect of frog toxin on voltage-gated sodium channel

A

Batrachotoxin causes sodium channels to open at more negative potentials and stay open much longer than usual, scrambling the info encoded by the action potentials

106
Q

What do voltage-gated potassium channels oepn in response to

A

Depolarisation of the membrane- there is a 1msec delay in them opening

107
Q

Why did Hodgkin and Huxley call the voltage-gated K+ conductance the delayed rectifier

A

There is a 1msec delay, and the K+ conductance out the cell due to the electrical driving force resets the membrane potential

108
Q

What voltage does the membrane potential rise to in an action potential

A

Around 40mV, around E Na

109
Q

How is the action potential actively propagated along the axon

A

The influx of positive charge at one region of the axon spreads inside the axon to depolarise the adjacent segment of membrane and continue the propogation

110
Q

What is orthodromic conduction

A

Action potential conduction from soma to axon terminal

111
Q

What is antidromic conduction

A

Action potential propagating backwards, elicited experimentally

112
Q

What is the typical rate of action potential velocity

A

10m/sec

113
Q

How does Lidocaine (local anaesthetic work)

A

Prevents action potentials by binding to the voltage-gated sodium channels, preventing the flow of Na+ that usually depolarises the channel

114
Q

Why are smaller axons affected by local anaesthetics before larger axons

A

In smaller axons, more of the voltage-gated sodium are required to work to ensure the action potential doesn’t fizzle out as it conducts down the axons

115
Q

Demyelinatnig disease thats not MS

A

Guillain-Barre syndrome- attacks the myelin of peripheral nerves that innervate muscle and skin, causing slowed/failed action potential firing in the axons innervatnig the muscles, causing profoundly slowed response times

116
Q

What is the axon hillock often called

A

The spike-initiation zone

117
Q

How does the spike initiation zone in sensory neurons differ fro typical neurons in the brain/spinal cord

A

In most sensory neurons, the spike initiation zone occurs near the sensory nerve endings, where depolarisation caused by sensory stimulation leads to the geenration of action potentials that propagate along the sensory nerves

118
Q

How does synaptic input cause generation of action potentials in typical neurons in the brain/spinal cord

A

Depolarisation of the dendrites and some caused by synaptic input leads to the generation of action potentials if the membrane of the axon hillock is depolarised beyond threshold

119
Q

How can the gating of voltage-sensitive channels be influenced by intracellular ion concentration eg Ca2+

A

In some cels, increased intracellular Ca2+ conc increases the probability that calcium-sensitive K+ channels open, but can also inactivate Ca2+ channels, so can have opposing effects

120
Q

How can excitability propertirs vary among differenr neurons

A

Some cellsshow a constant firing frequency in response to constant excitatory input, while some show decelerating/accelerating trains
Some neuron firing rates increase with small changes in input, while some require large input changes

121
Q

How does the spatial distribution of channel types in different regions of neurons vary with a direct bearing on function

A

eg dendrites/cell body/axon hillock/nerver terminal contain a greater variety of channels than the axon, because the input and output zones actively transform the signals they receive, while the axon is a simple relay line between these zones

Human basic neuroscience (68 decks)

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