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a. SL12100: Health and disease > L18 - Introduction To Nerve Cells & Excitability: Action Potential > Flashcards

L18 - Introduction To Nerve Cells & Excitability: Action Potential Flashcards

1
Q

How do neuron communicate between each other?

A

Dendrites and axons

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2
Q

What is an action potential?

A

Bried change in the V across the membrane due to flow of certain ion in and out of the neuron

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3
Q

What are APs like?

A
  • large (~100mV) transient changes (reversal)
  • rapid (1-4ms)
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4
Q

What can AP repeat at frequencies of?

A

Several hundrer per second
- depens on several ion channels

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5
Q

What are AP also known as?

A

Spikes, nerve impulses, nerve discharges

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6
Q

What is the all or none law?

A

If a stimulus is strong enough, AP occurs and a neuron sends info down an axon
- AP always a full response

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7
Q

What does changes in cell polarisation result in?

A

The signal being propagated down the length of the axon

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8
Q

What are the phases of APs?

A
  • hypopolarisatoin
  • depolarisation
  • overshoot
  • repolarisation
  • hyperpolarisation/undershoot
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9
Q

What happens during hypopolatisation?

A

Initial increase of the MP to the value of the threshold potential

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10
Q

What happens during depolarisation?

A

Potential moving from RMP to less negative values

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11
Q

What happens during overshoot?

A

Peak of AP (+40mV)

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12
Q

What happens during repolarisation?

A

Potential moving back to RMP (-70mV)

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13
Q

What happens during hyperpolarisation/undershoot?

A

Potential moving away from the RMP in a more negative direction

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14
Q

What do AP depend on?

A

VG ion channels
- responsible for initiation (Na+) and termination (K+) AP

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15
Q

How do VG channels work?

A
  • closed at RMP
  • open when depolarised
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16
Q

What triggers the opening and closing of VG ion channels?

A

Opening - change in V

Closing - return to RMP

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17
Q

What is the sequence of evens in an AP?

A
  • RP: VGNC and VGKC closed
  • stimulus = depolarisation to threshold, VGNC open
  • Na+ flows in, depolarises, more VGNC open
  • VGNC inactivated, Na+ slows, VGKC opens, K+ flows out = repolarisation begins
  • VGNC close, VGKC remain open = delayed hyperpolaritsation
  • RP restored
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18
Q

What are the properties of VGNC channels?

A
  • open rapidly with depolarisation
  • inactivation gate rapidly block Na+ permeability

Inactivated channels
- blocked during continued depolarisation
- move to closed state on repolarisation

19
Q

What are the properties of VGKC channels?

A
  • open slowly during depolarisation
  • channels remain open during depolarisation
  • close slowly on repolarisation
20
Q

What are the types of refractory periods?

A
  • absolute refractory period
  • relative refractory period
21
Q

What is the absolute refractory period?

A

AP not evoked
- VGNC inactivated
= cannot be reactivated until membrane repolarised and RP restored

22
Q

What is the relative refractory period?

A

Membrane potential hyperpolarise by VGKC
AP can be generated
- if stimulus strength strong enough to overcome hyperpolarisation to reach threshold

23
Q

What are the sequences of steps in AP propagation?

A
  • stim at A exceeds threshold for an AP, current spreads further along axon
  • current exceeds threshold, opens VGNC = generates AP at B

Repeats along axon

24
Q

What prevents back-propagation?

A
  • VGNC inactivation
  • open VGKC
25
Q

What is the velocity of an AP propagation depend on?

A

Upon axon diameter (size) and myelination

26
Q

How are axon diameter (size) and myelination involved in the velocity of AP propagation?

A

Large axon - less resistance to local current
Larger diameter - faster propagation
Myelination - insulates, local currents spread further

27
Q

What is saltatory conduction, and what is the VGNC and VGKC like?

A

The moving of local current from nodes of ranvier to another due to insulation

  • VGNC and VGKC at nodes of ranvier
28
Q

What are the sequences of steps in saltatory conduction?

A
  • sim exceeds threshold at node of ranvier
  • local current opens VGNC = AP at node B

Process repeated at node C

29
Q

What are examples of demyelination diseases?

A
  • guillian-barre syndrome
  • multiple sclerosis (MS)
30
Q

What is guillian-barre syndrome?

A

The destruction of schwann cells in PNS

31
Q

What is MS?

A

Cause by a loss of oligodendrocytes (in brain and spinal column)

32
Q

What do demyelination diseases involve?

A
  • muscle weakness
  • numbness or tingling
33
Q

What happens when the myelin coating of nerves degenerates?

A

Signals are diminished or completely destroyed

34
Q

What happens if the myein coating of nerves degenerate at nerves that are afferent fibres?

A

Numbness or tingling

35
Q

What happens if the myelin coating of nerves degenerate at nerves that are efferent fibres?

A

Weakness
- brain is expending a lot of energy but unable to move affected limbs
(Longest nerves, the more myelin that can be potentially be destroyed)

36
Q

What are graded potentials?

A

Changes in membrane potential confined to a small region of the membrane

37
Q

What does the magnitude of the potencial change vary to?

A

The strength of stimulus

38
Q

What are the two types of graded potentials?

A
  • excitatory
  • inhibitory
39
Q

What are the types of graded potential (summation)?

A
  • no summation
  • temporal summation
  • spatial summation
  • spatial summation of EPSPs and IPSPs
40
Q

What is the graded potential like with no summation?

A

2 stimuli separated in time cause EPSPs that do not add together

41
Q

What is the graded potential like with temporal summation?

A

2 excitatory stimuli close in time cause EPSPs that add together

42
Q

What is the graded potential like with spatial summation?

A

2 simultaenous stimuli at different locations cause EPSPs that add together

43
Q

What is the graded potential like with spatial summation of EPSPs and IPSPs?

A

Changes in the membrane can cancel each other out

a. SL12100: Health and disease (24 decks)

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