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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

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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
What is the velocity of an AP propagation depend on?
Upon axon diameter (size) and myelination
26
How are axon diameter (size) and myelination involved in the velocity of AP propagation?
Large axon - less resistance to local current Larger diameter - faster propagation Myelination - insulates, local currents spread further
27
What is saltatory conduction, and what is the VGNC and VGKC like?
The moving of local current from nodes of ranvier to another due to insulation - VGNC and VGKC at nodes of ranvier
28
What are the sequences of steps in saltatory conduction?
- sim exceeds threshold at node of ranvier - local current opens VGNC = AP at node B Process repeated at node C
29
What are examples of demyelination diseases?
- guillian-barre syndrome - multiple sclerosis (MS)
30
What is guillian-barre syndrome?
The destruction of schwann cells in PNS
31
What is MS?
Cause by a loss of oligodendrocytes (in brain and spinal column)
32
What do demyelination diseases involve?
- muscle weakness - numbness or tingling
33
What happens when the myelin coating of nerves degenerates?
Signals are diminished or completely destroyed
34
What happens if the myein coating of nerves degenerate at nerves that are afferent fibres?
Numbness or tingling
35
What happens if the myelin coating of nerves degenerate at nerves that are efferent fibres?
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
What are graded potentials?
Changes in membrane potential confined to a small region of the membrane
37
What does the magnitude of the potencial change vary to?
The strength of stimulus
38
What are the two types of graded potentials?
- excitatory - inhibitory
39
What are the types of graded potential (summation)?
- no summation - temporal summation - spatial summation - spatial summation of EPSPs and IPSPs
40
What is the graded potential like with no summation?
2 stimuli separated in time cause EPSPs that do not add together
41
What is the graded potential like with temporal summation?
2 excitatory stimuli close in time cause EPSPs that add together
42
What is the graded potential like with spatial summation?
2 simultaenous stimuli at different locations cause EPSPs that add together
43
What is the graded potential like with spatial summation of EPSPs and IPSPs?
Changes in the membrane can cancel each other out
44
What is the slowest sensations our bodies can send?
Pain - smaller fibers without myelin
45
What are the fastest signals in our bodies sent by?
Larger, myelinated axons found in neurons that transmit the sense of touvh or proprioception

a. SL12100: Health and disease (54 decks)

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