Session 4 - Action Potentials Flashcards

1
Q

What is an action potential?

A

A change in voltage across a membrane

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2
Q

What does an action potential depend on to be generated?

A

Ionic gradients and relative permeability

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3
Q

What is required to be reached for an action potential to be generated?

A

A threshold voltage level

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4
Q

What is meant by the “all or nothing” theory of action potential generation

A

Action potentials are either generated or they are not, there are no half or double action potentils

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5
Q

What is the basis of the all or nothingsystem?

A

The positivefeedback loop, whereby the membrane depolarizes, causing more Na+ channels to open, which means more Na+ enters cell which means the membrane depolarizes further leading to more Na+ channels opening - and so on.

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6
Q

Outline the sodium hypothesis

A

Once the membrane has been depolarised to threshhold voltage, voltage gated Na+ channels open, allowing Na+ influx as ions attempt to move to their equilibrium potential of +61 mv. This influxdeploarises the membrane further, causing more voltage gated Na+ channels to open.

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7
Q

What two events occur to cause repolarisation?

A

During maintained depolarisation, Na+ channels close by a mechanism called inactivation. Voltage gated K+ channels are opened by depolaristion, causing a K+ ion efflux as K+ attempts to move towards it own equilibrim potential.

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8
Q

What is A?

A

Na+ channels open

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9
Q

What is happening at B?

A

Reducing Na in cell makes ENa more negative

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10
Q

What is C?

A

Na+ channels close due to inactivation

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11
Q

What is D?

A

K+ channels open

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12
Q

Why can an action potential not be stopped halfway?

A

Because once threshold voltage reached, positive feedback of voltage gated sodium ion channels guarantees action potential synthesis.

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13
Q

What is the absolute refractory period?

A

Nearly all Na+ channels in inactivated state. Excitability is 0.

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14
Q

What is relative refractory period?

A

Na+ channels re recovering from inactivation, the excitbility returns towards normal as the number of channels in the inactive state decreses.

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15
Q

Howare Na+ channels inactivated?

A

By N-peptide binding

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16
Q

What is accomadation?

A

The longerastimulus is, the larger the depolarisation necessary to initiate an action potential.This is because Na+ channels become inactivated.

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17
Q

Describe the structure of voltage gated Na+ and Ca2+ channels

A

1 peptide with 4 homologous repeats Each repeat consists of 6 transmembranous domains 1 domain is able to sense the voltage field across a membrane Function required 1 subunit

18
Q

Describe the structure of voltage gated K+ channels

A

Four non=linked peptide repeats Six Transmembrane Domains One Domain is Voltage Sensitive Function requires Four subunits

19
Q

How do local anaesthetics prevent action potential generation?

A

Bind and block Na+ channels, stopping action potential generation

20
Q

In what order do local anaesthetics block nerve fibres?

A

1.Small myelinated axons 2.Non-myelinated axons 3.Large myelinated axons

21
Q

Why do local anaethetics effectneurones in this order?

A

Because they effect sensory neurones before motor

22
Q

At what point do LA’s block Na+ channels?

A

When the channel is open

23
Q

What can extracllular recording of action potentials give information about?

A

Conduction velocity under various conditions

24
Q

How can extracellular recording be used to measure conduction velocity?

A

Electrodes are used to raise the membrane potential to threshold to generate an action potential. Changes in potential between stimulating (Cathode, -‘ve) and recording (Anode,+’ve) electrodes along an axon.

25
Q

How can conduction velocity be calculated?

A

Using the equation conduction velocity = distance between electrodes /time gap between the stimulus and the action potential being generated

26
Q

How are axons raised to threshold?

A

Arrival of a stimulus causes voltage dependent Na+ channels to open

27
Q

What is the local circuit theory of propagation?

A

Change in membrane potential at one part of axon spreads to adjacent areas via local current spread. Local current spread causes depolarisation of adjacent membrane and opening of voltage gated sodium ion channels, causing the propagation of the action potential.

28
Q

What is the relationship between the distance the local current spreads and the speed of the concuction velocity of the axon

A

Further the spread, the faster the conduction velocity of the axon

29
Q

What are three properties of an axon which lead to high conduction velocity?

A
  • A high membrane resistance - A high axon diameter (low cytoplasmic resistance) - A low Membrane capacitance
30
Q

How does a high membrane resistance lead to high conduction velocity?

A

???? Can anyone clarify this in their notes? The lower the resistance, the more ion channels open. Lower the resistance > more ion channels open > more loss of local current across the membrane > limits local current spread

31
Q

How does low membrane capacitance led to high conduction velocity?

A

Measure of the ability of the lipid bilayer to store charge. High capacitance requires more current to charge (or a longer time for a given current). Can cause a decrease in local current spread.

32
Q

What is increased by myelination?

A

Conduction velocity

33
Q

What type of axons are myelinated?

A

Large diameter axons such as motor neurones, smaller ones such as sensory neurones are not.

34
Q

How does myelination increase conduction velocity?

A

Reduces capcitance and increases Membrane Resistance. This is achieved via saltatory propagation.

35
Q

Where do action potentials occur on a myelinated neurone?

A

Nodes of ranvier

36
Q

What is saltatory propagation?

A

AP jumps between nodes of ranvier because myelin sheath acts as good insulator, so local circuit currents depolarise next node along and generate further AP

37
Q

What is the density of Na+ ion channels at the nodes of ranvier? How does this differ from sensory neurones?

A

High Sensory neurones have even distribution

38
Q

What two types of cells are responsible for myelination?

A

Schwanncells and oligodendrocytes

39
Q

What are the consequences of demyelination, as in MS?

A

Insufficient number of Na+ channels at demyelinated regions, which reduce or block conduction velocity of action potentials.

40
Q

Give a local anesthetic example

A

Procine blocks na chanalls

41
Q

Synaptic tramesion types of synpase

A

Axo axonal Axodendretic Axosomatic