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SA ICPP > S7) The Action Potential & Neuromuscular Junction > Flashcards

S7) The Action Potential & Neuromuscular Junction Flashcards

1
Q

What is an action potential?

A

An action potential is a change in voltage across the cell membrane

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2
Q

What are the properties of action potentials?

A

Action potentials:

  • Depend on ionic gradients and relative permeability
  • Only occur if a threshold level is reached
  • Are propagated without loss of amplitude
  • all or nothing
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3
Q

Describe the sodium hypothesis of the action potential

A

1 - Threshold potential reached

2 - Na+ channels open

3 - Na+ channels inactivate & K+ channels open

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4
Q

Explain the term threshold potential

A
  • Threshold potential is the critical level to which a membrane potential must be depolarised to initiate an action potential
  • Once this membrane potential is reached, a positive feedback occurs as Na+ channels begin to open
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5
Q

Depolarisation is followed by repolarisation.

What happens during this process?

A
  • Potassium channels open causing an efflux of K+
  • Sodium channels inactivate stopping the influx of Na+
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6
Q

What is the absolute refractory period?

A

The absolute refractory period is the time between the initial opening and subsequent closing of the Na+ channels (approx. ~1 millisecond in nerves)

  • no stimulus can create an action potential no matter how strong
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7
Q

What is the relative refractory period?

A

The relative refractory period is the time needed for Na+ channels to recover back to their resting membrane potential so they can open again (approx. 4 milliseconds)

  • strong stimulus can generate an action potential
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8
Q

Local anaesthetics act by binding to and block Na+ channels, thereby stopping action potential generation.

How is this achieved?

A
  • Most local anaesthetics are weak bases and cross the membrane in their unionised form
  • They block Na+ channels easily when the channel is open
  • They also have a higher affinity for the inactivated state of the Na+ channel
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9
Q

In what order do local anaesthetics block the conduction in nerve fibres?

A
  • Small myelinated axons
  • Non-myelinated axons
  • Large myelinated axons
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10
Q

What is electrical stimulation and how is it done?

A

- Electrical stimulation is used to stimulate an axon / group of axons to threshold potential, thus intiating an action potential

  • Stimulation occurs under a cathode (negatively charged)
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11
Q

How does one calculate conduction velocity?

A

Conduction velocity = distance / time

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12
Q

How is an action potential conducted along an axon?

A
  • A change in membrane potential in one part can spread to adjacent areas of the axon by local currents
  • When local current spread causes depolarisation of part of the axon to threshold potential then an action potential is initiated in that location
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13
Q

What are the properties of the axon that lead to a high conduction velocity?

A
  • A high membrane resistance
  • A low membrane capacitance
  • A large axon diameter
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14
Q

What is capacitance?

A

Capacitance is the ability of a lipid bilayer to store charge

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15
Q

Why does a low capacitance lead to a faster conduction velocity?

A
  • A high capacitance takes more current to charge
  • It can cause a decrease in local current spread
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16
Q

What is membrane resistance?

A

The membrane resistance is a function of the number of open ion channels

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17
Q

Why does a low membrane resistance lead to a slower conduction velocity?

A

The lower the resistance, the more ion channels are open and the more loss of local current occurs across the membrane

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18
Q

Local currents cause an action potential to propagate down an axon.

Why do action potentials not move backwards?

A

The action potential will not move backwards because the area of axon that has just fired an action potential is refractory and cannot fire another action potential until it has recovered from being refractory

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19
Q

Explain how the myelin sheath affects conduct velocity

A

Myelin reduces the capacitance and increases the resistance of the axonal membrane, hence increasing the overall conduction velocity

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20
Q

Identify the cells which form myelin and describe their actions

A
  • Schwann cells myelinate peripheral axons
  • Oligodendrocytes myelinate axons in the CNS
21
Q

Describe the process of saltatory conduction in myelinated nerve fibres

A
  • Saltatory conduction is the propagation of action potentials along myelinated axons from one node of Ranvier to the next node
  • This increases the conduction velocity of action potentials
22
Q

What is the relationship with fibre diameter and conduction velocity?

A
  • Myelinated fibres: velocity proportional to diameter
  • Unmyelinated fibres: velocity proportional diameter1/2
23
Q

In terms of myelination & conduction velocity, describe what occurs in multiple sclerosis?

A

Multiple sclerosis is an autoimmune disease wherein the myelin is destroyed in certain areas of the CNS, leading to decreased conduction velocity and/or the complete block of action potentials

24
Q

describe repolarisation

A

1. delpolarisation

  • Na channels inactivated
  • K channels activated

2. Repolarisation

  • Na influx stopped
  • k efflux
25
Q

conductance

A

conductance for a particular ion represents an increase in the number of ion channels open

26
Q

Henderson - Hasselbalch eq

A
27
Q

molecular nature of Na, ca, K channels

A
  • 4 homologous repeats = 1 subunit
  • each repeat consists of 6 transmembrane spanning domains

K channels

  • same apart from each repeat is a seperate subunit
28
Q

fibre diameter and conduction velocity

A

There are several Na channels in the nodes of ranvier but very few under the mylein sheath

29
Q

Axon hillox

A

dendrites = where depolarisation initiated

axon hillock = initiation of an AP

30
Q

why is it important that sodium channels become inactivated

A

1) stop influx of Na
2) they cant open again so it stops action potential going back in reverse

31
Q

consequence of delayed closing of K channels

A

membrane potential will hyperpolarise more and increase recovery faster

32
Q

why is the Na/Kaptase not involved in producing the action potential

A

dont get much of a change in the ionic concs and the change you do get is small

33
Q

summary of an action potential

A

1) depolarisation to threashold triggers more sodium volted gated channels to open
2) Na influx = A.P
3) depolarisation inactivates NA channels
4) K channels open and efflux of K = repolarisation (membrane potential moves towards Ek)
5) small movement of Na/K so NA/K ATPase not involved

34
Q

how to increase membrane potential

A

high membrane resistance

low membrane capitcance

  • longer the distance the faster the conduction
35
Q

feature of a myelinated axon

A

high membrane resistance and low membrane capacitance

36
Q

comparison of calcium at intracellular and extracellular levels

A

intracellular (100nM) < extracellular (1-2mM)

movement of Ca into the cell initiates many cellular events

37
Q

why do voltage gated calcium channels open

A

when the action potential arrives at the nerve terminal depolarisation opens them

They enter the cell

38
Q

role of Ca influx

A

stimulates the release of neurotransmitter

39
Q

clincal use of nifedipine

A

treats high blood pressure

reduces Ca entry into smooth muscle cells

  • relaxes the blood vessels and allows more blood to pass
40
Q

order of ca events

A
  1. Ca enters via voltage gated Ca channels
  2. Ca binds to synaptotagnin
  3. vesicles brought close to membrane
  4. snare complex makes fusion pores
  5. neurotransmitter released
41
Q

Ach Receptors

A

Ach binds to nicotinic receptors on post junctional muscle membrane = deoplarisation (end - plate potential)

= rasies the adjacent membrane above threashold = action potential

42
Q

what is the neuromusclar junction

A

synpase between a nerve and skeletal muscle fibre

43
Q

neuromuscular blockers

A
  • competitive block
  • depolarising block (slows maintained depolarisation which inactivates na channels and maintians depolarisation)
44
Q

depolarising block by succinylcholine

A
  • NORMALLY breif depolarisation activates adjacent Na channels due to local spread of charge = AP
  • succinlycholine - cant create an AP and maintains the refactory period ( no AP)
45
Q

mayasthenia gravis

A

autoimmune targeting nACh receptors

  • weakness
  • antibodies directed againts nAChR on postsynaptic membrane of skeletal muscle = loss of functional nAChR by compliment mediated lysis and receptor degregation
  • threashold for action potential cant be met
46
Q

d-tubocurarine

A

competitve blocker of nACh

  • paralysis
47
Q

organophosphate poisoning

A
  • insectisisdes
  • acetylcholineesterase inhibitors form unstable covalent bonds
48
Q

nAChR v mAChR

A

nAChR - fast depolarisation as its ligand gated

mAChR - slower response as they are coipled to G protein receptors which trigger events in a cell

SA ICPP (11 decks)

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