Lecture 7: Action Potentials Flashcards

1
Q

Opening and closing of any gate is _____.

A

probabilistic

ie. at intermediate voltage (like -50mV), some fraction of K-channels will have open n-gates, and some will not

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2
Q

Does m gate or n gate opens faster?

A

’m’ gate (Na) opens faster than the ‘n’ gate (K)

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3
Q

When is each gate (m, h, n) more likely to be open?

A

m: positive potentials
h: negative potentials
n: positive potentials

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4
Q

Why does the K+ conductance not need to have an inactivation gate of its own?

A

K+ itself is negative feedback – just by going through its channels will make its own channels inactivate because it’s making the membrane potential more negative, which closes the n gate

because K+ is moving the membrane potential in the opposite direction of Na+, it does not need an inactivation gate because it is its own activation gate

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5
Q

Why does the Na+ conductance need to have an inactivation gate of its own?

A

the more Na+ that enters, the more depolarized the membrane potential will be – need an external mechanism (h gate) to stop Na+ from entering

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6
Q

Can we explain each phase of a real world AP?

A

yes

  • depolarization is about extra Na+ conductance
  • repolarization is about Na+ conductance going away, and K+ conductance starting
  • hyperpolarization is about K+ conductance staying on for some time, even though it returns to RMP and threshold potential
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7
Q

What’s happening at VTh to cause accelerating depolarization?

A

accelerating depolarization is positive feedback cycle for Na+ channels – every few channels that open, open more channels for current to flow

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8
Q

Why is there a refractory period after an AP is fired (before another one can be generated?)

A

refractory period is explained by features of the h gate

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9
Q

How does that all work so quickly?

A
  • not able to explain with H&H’s data

- only channels can explain how so much charge can move across membrane so quickly – transporters are not enough

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10
Q

What is the problem with action potentials?

A

action potentials are very large depolarizations, and when triggered they move a lot of ions (both Na+ and K+) across the membrane

  • those ions eventually have to be pumped back the other way, and that’s energetically expensive
  • they also reduce rich analog, graded information to a binary ‘fire or don’t fire’
  • are metabolically wasteful
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11
Q

What is myelin?

A

substance containing high levels of lipid and proteins, produced in myelinating glia, which form outgrowths that wrap around neural axons in CNS and PNS (up to 16-20 layers)

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12
Q

What is the function of myelin?

A

provides electrical insulation for axons

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13
Q

What does myelination produce? What does it reduce?

A

very tiny extracellular space between myelin and axon membrane

severely reduces the expression/function of ion channels below it

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14
Q

What does myelination interfere with?

A

layers of insulation interferes with ability of axon membrane to act as capacitor (ie. storing charge when current flows)

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15
Q

What does myelination allow?

A

allows electrotonic current to spread more efficiently, increasing depolarization rate

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16
Q

How does myelination affect Rm and Ri, and the length constant?

A

increases Rm (due to fewer leaking channels) without affecting Ri, therefore λ will greatly increase

  • current will spread much more efficiently, compared to an unmyelinated axon
  • this allows the AP related depolarization to travel much further by electrotonic conduction before needing to be regenerated
17
Q

What are myelinated stretches of axons punctuated by?

A

VG-channel dense Nodes of Ranvier

18
Q

Where are voltage-gated sodium channels in a myelinated axon found?

A

centre of nodes of Ranvier

19
Q

Where are voltage-gated potassium channels in a myelinated axon found?

A

outer parts of nodes of Ranvier

20
Q

What is saltatory propagation?

A

AP appears to jump abruptly from node to node because new APs can only be generated where there are VG-Na channels (ie. not in the internode regions)

21
Q

When does AP regenerate during saltatory conduction?

A

at each node – even before the potential has finished spreading in the internode

22
Q

Where does current decay during saltatory conduction?

A

in the internodal (myelinated) region

23
Q

How does the magnitude of AP change throughout saltatory conduction?

A

magnitude of the AP-associated current decreases gradually between nodes then abruptly jumps back to full strength as the AP is regenerated at the next node

24
Q

Is there a trade-off to myelination?

A

you now have to grow and look after a whole new class of cells, in addition to neurons

ie. multiple sclerosis (MS) – autoimmune disease that causes immune system to attack oligodendrocytes within CNS, leading to losses of myelination of CNS axons

25
Q

How is myelination affected due to multiple sclerosis (MS)?

A
  • immune system attacks oligodendrocytes within CNS, leading to losses of myelination of CNS axons
  • demyelinated axons are no longer insulated in the former internode regions (leaky), which can slow APs or even lead to complete failure of AP transmission in the affected axons if the VGNCs at the next node can’t get depolarized enough to reach threshold and regenerate the AP