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ESA 2 > M&R session 4: action potentials and the cellular response > Flashcards

M&R session 4: action potentials and the cellular response Flashcards

1
Q

Describe an action potential

A

A rapid change in the voltage across a membrane.
Depends on ionic gradients and relative permeability
Only occurs if a threshold level is reached: all or nothing
Propagated without loss of amplitude

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2
Q

How do action potentials in neurones, skeletal muscle, SA nodes and cardiac ventricles differ?

A

Draw a diagram :)

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3
Q

How is an action potential generated?

A

An increase in permeability to Na+ bringing the membrane potential closer to ENa (sodium hypothesis). Conductance of an ion is dependent on the number of open channels. If conductance is increased, the MP (Vm) will move closer to Eion.

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4
Q

How many ions need to flow to generate an action potential?

A

Q=CmV (Cm=1uFcm^-2)
100mV AP (0.1V), Q=(110^-6)0.1= 110^-7
F=96500 C per mol
Amount of ions moving is (110^-7)/96500=1*10^-12 mol cm^-2
Change in concentration=mol/volume
so
Change in conc= (amount of ions moving * area) / (volume)

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5
Q

How can the generation of an AP be investigated?

A
  1. Using different [ions] to assess the contribution of different ions
  2. Patch-clamping: enables currents flowing through individual ion channels to be measured
  3. Voltage clamping: controls Vm so that the ionic currents can be measured. Allows measurement of membrane current at a constant voltage
    - in a clamped cell the change in membrane voltage in response to membrane current is prevented
    - can see the effect of voltage on Na+ & K+ channels
    - both inside and outside the cell
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6
Q

What does voltage-clamping show about sodium and potassium ion channels?

A

K+ channels open more slowly than Na+channels and do not close immediately (take time to close on repolarisation
Na+ goes into the cell, usually leads to depolarisation (but not when voltage clamped as controlling current). Sodium current wanes to 0: inactivated state, channels will not open before they have had a chance to recover

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7
Q

Describe the time course of conductance changes during an action potential

A

Draw diagram

Lec 4.1 slide 10

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8
Q

What happens during the upstroke of an AP (depolarisation)?

A
  1. Depolarisation to threshold initiates AP at the axon hillock (EPSP if doesn’t reach threshold)
  2. Na+ channels open, Na+ enters cell
  3. Positive feedback basis of all or none characteristic: more Na+ enters cell as it tries to move Vm to ENa
  4. Membrane depolarises
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9
Q

What happens in the downstroke of the AP (repolarisation)?

A

Following depolarisation:
1. K+ channels are opened causing K+ efflux
2. Na+ channels are inactivated, Na+ influx stops
Both of these cause repolarisation

Na+-K+-ATPase is not involved in repolarisation: just works in the background to ensure a stable supply of ions

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10
Q

What is the absolute refractory period and what property does it confer on nerve cells?

A

Inactivated Na+ channels prevent another action potential occurring straight away, allowing the resting MP to be re-established.
All Na+ channels are inactivated, so it is impossible to re-fire an AP, no matter how strong the stimulus is.

Prevents re-entrant excitation, and gives directionality in impulse propagation

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11
Q

Explain the concept of accommodation

A

The longer the stimulus, the larger the depolarisation needed for an AP, so the threshold becomes more positive and is eventually no longer reached as stimuli of slowly increasing intensity are applied
This is because it increases the number of inactivated Na+ channels, as the voltage-gated Na+ channels cannot detect slow progressive depolarisation

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12
Q

How does the neurotoxin tetrodotoxin work?

A

Blocks the movement of Na+ into a cell by binding to voltage-sensitive Na+ channels, therefore blocks action potential upstroke
Toxin found in pufferfish
Small amounts sufficient to cause death by respiratory failure, as will paralyse the diaphragm

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13
Q

Describe the basic structure of voltage-gated Na+ channels (lec 4.1 slide 17)

A

Functional channel-1 alpha subunit

Each channel has 6 hydrophobic membrane-spanning domains:

  • 4: voltage sensor. The 4th in each has a high no. positive amino acids to detect the voltage field across the membrane
  • Between 5 and 6: pore/H5 region. Change in MP will cause a conformational change in this area
  • between 6 and the next 1: inactivation particle. When pore is closed it just sits there, but when open it can swing into the pore and block it so that Na+ can’t move through. “Ball and chain”
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14
Q

Describe the basic structure of voltage-gated K+ channels

A

Smaller but otherwise similar to Na+. Need 4 alpha subunits for a functional channel

  • P (or H5) region contributes to selectivity
  • S4 has positive aas contributing to voltage sensitivity
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15
Q

How to voltage gated channels open and close?

A

In a random manner

Don’t all close at the same time

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16
Q

In what order to local anaesthetics block axons?

A

1st: small unmyelinated axons
2nd: unmyelinated axons
3rd: large myelinated axons

i.e. pain fibres before motor fibres
Block voltage gated sodium channels so sodium can’t influx to cause depolarisation

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17
Q

How does the lipid solubility of the drug affect pathways used?

A

Relative importance of hydrophobic and hydrophilic pathway varies according to the lipid solubility of the drug
Hydrophilic pathway is use-dependent: e.g. the more stitches after local anaesthetic, the less sensation
Hydrophobic pathway is none use-dependent

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18
Q

Describe the actions of procaine

A

Binds and blocks Na+ channels so stops AP generation
Weak bases, cross membrane in unionised form
Easier to block Na+ channels when open, but have increase affinity to inactivated form. Lower pH=higher charge=block better

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19
Q

State the different classifications of peripheral axons

A

A alpha: sensory. From Muscle spindles, motor neurones and skeletal muscle
A delta: seonsry from sharp pain and temp. receptors
B: preganglionic neurones of the ANS
C: sensory fibres from diffuse pain, temperature and itch receptors

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20
Q

Name 4 diseases affecting conduction of the AP due to damaged myelin sheath

A

CNS:

  • multiple sclerosis (all CNS nerves)
  • Devic’s disease (optic and spinal cord nerves)

PNS:

  • Landy-Guillain-Barre syndrome
  • Charcot-Marie-Tooth disease
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21
Q

How is extracellular recording carried out?

A

Excitability is increased under a cathode (-ve) to stimulate an AP by stimulating an axon to threshold. Anode decreases excitability.
Gives conduction velocity information under various conditions

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22
Q

What is diphasic recording?

A

Shows when depolarisation reaches the anode and cathode.

The difference between two points on an axon

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23
Q

What is monophasic recording?

A

Easier to record. A part of an axon is damaged, so the AP stops at this damaged region, and can detect this change

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24
Q

How is conduction velocity calculated?

A

Distance between stimulating and recording electrode divided by the time between the stimulus and AP being registered by the recording electrode

25
Q

What is the local current theory?

A

Injection of current into an axon will cause the charge to spread along the axon and cause an immediate local change in membrane potential
The change in Vm spreads due to local current: tends to repel opposite charges
Conduction velocity is determined by how far along an axon these local currents can spread
When local current spread causes depolarisation to threshold in that part of the axon, an AP is initiated

26
Q

What is axon resistance determined by?

A

The number of ion channels open.
Fewer channels open=higher resistance. Higher resistance=longer length constant so faster conduction, as depolarisation can spread further along the axon
Low resistance, more ion channels open, more loss of local current across membrane, so local current effect is limited

27
Q

What is axon capacitance?

A

The ability to store charge.

A high capacitance takes more current to charge/longer time for a given current so decreases local current spread

28
Q

What effect will decreasing capacitance have?

A

Increase speed at which the charge will cause an action potential

29
Q

How can an axon have a high conduction velocity?

A
  • High membrane resistance
  • Low membrane capacitance
  • Further local current spread down axon
  • Large axon diameter (so low cytoplasmic resistance)
  • Longer length constant
30
Q

What is the length constant (lambda) of an axon?

A

The distance for an AP to fall to 37% of its original value

31
Q

When do axons start to become myelinated?

A

At about 4 months of foetal development

32
Q

How are axons myelinated in different areas of the body?

A

Peripheral axons-by Schwann cells
CNS axons-by oligodendrocytes

Both types of cells wrap concentrically around the axon

33
Q

Which axons are myelinated?

A

Large diameter axons, e.g. motoneurones

Not small axons like C-fibre sensory neurones

34
Q

What effect does myelination have on axonal properties?

A

Decreases capacitance and increases resistance, both by ~100 fold

These both increase length constant and slightly decrease the time constant

35
Q

Describe saltatory conduction

A

Decreased internodal capacitance, so local current induced by nodes of Ranvier spreads further to depolarise the next node, without firing an AP in the internodal region. Local current spread is faster-increased conduction velocity
Nerve impulse in a “jumping” manner between nodes of Ranvier (unmyelinated regions)

36
Q

What is the optimum conduction velocity for a myelinated neurone?

A

d/D=0.7

where d is the axon diameter and D is the diameter of the whole neurone (including myelin)

37
Q

Why do APs only occur at nodes of Ranvier in myelinated axons?

A

Myelin is an insulator, nodes of Ranvier aren’t myelinated
They have a high density of Na+ channels here
K+ channels MAY be more widely distributed

38
Q

Describe conduction in unmyelinated axons

A

No saltatory conduction

Local current flow causes depolarisation to threshold, even distribution of Na+ channels along the axon

39
Q

How does myelination decrease capacitance?

A

Decreases dissipation of the local current, so permits more distant regions to be brought to the threshold for firing an AP

40
Q

What happens to an axon that is demyelinated in a disease process?

A

Local current is unable to raise to threshold

Density of the current decreases due to resistive and capacitative shunting

41
Q

What is the effect of conduction of nerve impulses immediately after the loss of the myelin sheath?

A

Conduction failure due to increased capacitance and current leak preventing nodal channels from being raised to threshold.

42
Q

What happens to nerve impulse conduction following demyelination, after a period of recovery?

A

Slightly increased rate of conduction, as ion channels are redistributed so not all concentrated at the previous nodes of ranvier. Slower conduction than normal, but the impulse is conducted

43
Q

Effect of depolarisation of neurone on voltage gated Ca2+ channels?

A

Opens
ECa=+122mV so big driving force for its entry. As intracellular Ca2+ is very low the open channels can raise the concentration significantly

44
Q

Describe the structure of voltage-gated Ca2+ channels

A

Similar to VG Na+ channels in that one peptide will produce a functional ion channel
4 subunits
Needs a pore-forming subunit to be functional
Extracellularly is glycosylated and intracellularly is phosphorylated

45
Q

What are the most common types of Ca2+ channels, where are they found and how are they blocked?

A

L-type. In smooth and skeletal muscle, neurones and lungs

Blocked by dihydropyridines to regulate blood pressure

46
Q

Describe exocytic neurotransmitter release at the NMJ

A

Ca2+ entry through Ca2+ channels
Ca2+ binds to synaptotagmin
Vesicle brought close to membrane
Snare complex makes a fusion pore, so inside of vesicle becomes continuous with extracellular space, so neurotransmitter can be released into synaptic cleft

47
Q

Release of ACh activates nAChRs: how does depolarisation occur?

A

Have an intrinsic ligand-gated ion channel with equal permeability for Na+ and K+, but due to the equilibrium potentials Na+ influx dominates, leading to depolarisation (driving force for K+ to leave is high because the membrane potential is close to EK)

48
Q

Describe the function of a nACh receptor

A

ACh binds to each alpha subunit on the post-junctional membrane, causing a conformational change in the nAChR so the pore opens
K+ and Na+ pass through causing depolarisation of skeletal muscle membrane: END PLATE POTENTIAL (on graph of AP is the point where it reaches threshold)
This raises muscle above threshold so that an AP is produced. End plate potential depolarises adjacent muscle membrane and activates voltage gated Na+ channels, initiating an AP in muscle fibre which contracts due to excitation-contraction coupling

49
Q

What happens to the end plate potential as external Ca2+ is lowered?

A

It decreases in amplitude

Because transmitter release is dependent on Ca2+ entry

50
Q

Curare (a non-depolarising blocker)

A

Common name for plant extract alkyloid poisons. Main toxin is d-tubocuranine
Causes paralysis by blocking transmission between nerve and muscle: blocks nAChR so NMJ blocked. Acts as a competitive antagonist.
Doesn’t cause conformational change in channel: stays closed
When injected/darted: ok to eat
Antidote: AChE inhibitor-by inhibiting breakdown increases circulating ACh concentration, so more ACh can bind to nAChR rather than curare

51
Q

Succinylcholine

A

A depolarising blocker used to induce muscle relaxation and short-term paralysis
Binds with nAChR and activates it, causing maintained depolarisation. This leads to accommodation, so Na+ channels near the NMJ are inactivated

52
Q

Miniature end plate potentials?

A

Spontaneous release of a small amount of neurotransmitter without Ca2+ present
Response of a single vesicle releasing ACh
Many MEPPs simultaneously will create an action potential in the post-synaptic membrane

53
Q

Myasthenia gravis?

A

Blockage of nAChR at the postsynaptic membrane, due to autoimmune attack that releases antibodies directed against the nAChR.
These cause loss of functional nAChR by complement-mediated lysis and receptor degradation
EPPs are reduced in amplitude causing muscle weakness and fatigue
MEPPs: each quantum of ACh released produces a smaller response than in normal muscle as there are fewer nAChR available

54
Q

What is the difference between activation and inactivation of a voltage gated ion channel?

A

Activation-closed channel opened due to a change in voltage as sensed by the channel
Inactivation-channel unable to open due to inactivation particle; must recover before can activate again

55
Q

What is the effect on the neurone of 4-aminopyridine?

A

Blocks voltage gated K+ channels so blocks the downstroke as K+ can’t re-enter the cell, so the membrane can’t repolarise

56
Q

Composition and properties of myelin

A

Phospholipid, cholesterol and protein

Electrical insulator

57
Q

What is Wallerian regeneration?

A

Some peripheral myelinated nerve fibres can regenerate from the central end if cut, at a rate of 1-3mm per day

58
Q

Distribution of ion channels in myelinated nerves?

A

~10000 Na+ channels at nodes of ranvier

K+ channels usually just underneath the myelin either side of the node

59
Q

Consequences for conduction due to depolarisation?

A

Partial demyelination: slower rate as fewer APs due to decreased resistance and increased capacitance
Complete demyelination: saltatory conduction stops; over time there is a redistribution of ion channels

Makes nerve fibres more difficult to stimulate with electrode currents

ESA 2 (58 decks)

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