Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ICPP > L5 Action potentials > Flashcards

L5 Action potentials Flashcards

1
Q

a) What is an action potential?

b) What are the properties of an action potential?

A

a) The change in voltage/ electrical potential across a membrane
b) - Depend on ionic gradients and relative permeability
- Only occur if a threshold level is reached
- Are propagated without loss of amplitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

a) If the conductance to an ion is increased what happens to the membrane potential?
b) What is conductance dependent on?

A

a) The membrane potential will move closer to the equilibrium potential for that ion
b) The number of channels for the ion that are open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain how the ionic permeability of the membrane alters with time and how this generates the action potential

A
  • The resting membrane of a cell is about -70mV (near to eqm potential of K+)
  • Threshold potential is reached and Na+ channels open causing Na+ ions to move in and hence the membrane potential moves closer to Eqm potential of Na (less negative i.e. depolarisation)
  • The na+ channels then become inactivated and K+ channels open causing K+ to move out and the membrane potential moves closer to the eqm potential of k+ becomes more negative i.e. repolarisation then hyperpolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

All or nothing principle?

A
  • no action potential is generated unless the threshold is reached
  • when it is reached every action potential will reach the same peak membrane potential (40mV) no matter how strong the stimulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between the a)Absolute refractory period and the b)Relative refractory period?

A

a) ARP: Period immediately following a fire and no new AP can be generated no matter the stimulus
- nearly all Na+ channels are in the inactivated state

b) RRP: contains recovering Na+ channels and voltage gated K+ channels begin to close
- it is possible to induce an AP but it has to be a very large stimulus to depolarise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline the basic structure of a voltage-gated Na+ channel

A
  • contains only one α subunit
  • the α has 4 similar sections or repeats (I-IV)
  • each containing six membrane-spanning segments, labelled S1 through S6.
  • the S4 segment acts as the channel’s voltage sensor.
  • The voltage sensitivity of this channel is due to positive amino acids located at every third position.
  • when there is a change in transmembrane voltage, this segment moves toward the extracellular side of the cell membrane, allowing the channel to become permeable to ions. (open)
  • There is a pore region and the inactivation particle will go into the pore to stop movement of ions –> inactivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline the basic structure of a voltage-gates K+ channel

A
  • one α subunit is 1/4 of a channel (i.e. only 1/4 of the na+)
  • a channel consists of 4 individual α subunits
  • each α subunit consists of 6 membrane-spanning domains
  • s4 voltage sensing region also detects the voltage and opens or closes the channel pore
  • no inactivation particle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to local anaesthetics work ?

A
  • Most local anaesthetics are weak bases and cross the membrane in their unionised form (membrane permeable)
  • They bing to and block Na+ channels easily when the channel is open
  • They also have a higher affinity for the inactivated state of the Na+ channel
  • Stopping action potential generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

a) Examples of local anaesthetics?

b) Order of blocking for local anaesthetics?

A

a) Lidocaine
b)
1. Small myelinated axons
2. un-myelinated axons
3. large myelinated axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does one calculate conduction velocity?

A

Conduction velocity = distance / time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is an action potential conducted along an axon?

A
  • Local current theory
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

a) What is membrane capacitance?

b) What is membrane resistance?

A

a) The ability to store charge
b) It is a function of the number of open ion channels
- lower resistance - more ion channels open
- higher resistance - less ion channels open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What factors increase conduction velocity of an AP and explain why?

A
  1. Large axon diameter
    - less resistance to ION flow (they have more space to travel and less likely to bump into something)
  2. LOW membrane capacitance
    - a high capacitance takes more current to charge (voltage changes more slowly) and would cause a decrease in local current spread
  3. HIGH MEMBRANE resistance
    - there would be less ion channels open and so less local currents would be lost across the membrane and the change in voltage would be able to spread further along the axon
  4. Myelination
    - AP jumps from node to node
    - increases memb resistance and decreases memb capacitance
17
Q

How does myelination affect the conduction velocity of a neurone?

A
  • Myelinated axon has faster conduction velocity:
  • -> axon surrounded by myelin sheath (comprised of schwann cells)
  • -> sheath is electrically insulating, it increases the speed of transmission of AP
  • -> there are gaps called nodes of ranvier which have a high density of Na+ channels where the AP is propagated by saltatory conduction: Local circuit currents depolarise the next node above threshold and initiate an AP
18
Q

Identify the cells which form myelin and describe their actions

A
  • Schwann cells myelinate peripheral axons

- Oligodendrocytes myelinate axons in the CNS

19
Q

a) What is demyelination?
b) What diseases cause this in the:
i) Central nervous system
ii) Peripheral nervous system

A

a) Breakdown or damage of the myelin sheath
b)
i) Multiple sclerosis (all CNS nerves) and Devic’s disease (optic and spinal cord nerves only)
ii) Landry-guillain-barre syndrome and charcot-marie-tooth disease

20
Q

Explain the affect that demyelination has on conduction velocity?

A
  • Demyelination causes inefficient saltatory conduction as depolarisation must also occur at the gaps in the myelinated sheath, decreasing the speed of impulse transmission.
  • failure to reach threshold
21
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

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

What is the Neuromuscular Junction?

A

The synapse between a nerve and a skeletal muscle fibre

24
Q

Outline the steps that occur at the nerve terminal (the presynaptic neurone).

A
  1. An AP arrives at the nerve terminal
  2. AP causes voltage-gated Ca2+ channels to open
  3. Ca2+ enters the nerve terminal down conc gradient
  4. Increased concentration of Ca2+ inside
  5. stimulates neurotransmitter vesicles to move towards and fuse with the presynaptic membrane
  6. Neurotransmitter (e.g. Ach) released from vesicles via exocytosis
25
Q

What ion channels are in the nerve terminal?

A
  • voltage gated NA+ channels
  • voltage gated K+ channels
  • voltage gated Ca2+ channels
26
Q

What will increase the amount of Ca2+ entering the nerve terminal?

A

an increase in frequency of Action potentials

27
Q

What actually causes the release of the neurotransmitter?

A
  1. AP arrives at nerve terminal, voltage gated Ca2+ channels open and ca2+ enters nerve terminal
  2. Ca2+ binds to synaptotagmin
  3. Neurotransmitter vesicle brought closer to membrane
  4. Snare complex makes fusion pores
  5. contents of vesicle diffuse into synaptic cleft
28
Q

Why is intracellular Ca2+ considered a cellular second messenger?

A
  • Normally intracellular ca2+ conc is very low and highly regulated
  • hence a small influx of IC ca2+ will cause a significant increase in ca2+ concentration and it can initiate many cellular events including release of neurotransmitters
29
Q

What is the function of acetylcholine esterase ?

A
  • it is an enzyme that breaks down ACh in the synapse

- if it wasnt broken down then it would cause the muscle to keep on firing (BAD)

30
Q

What does nAChR stand for and what is it/ where is it found?

A
  • Nicotinic acetylcholine receptor
  • it is a ligand gated ion channel that is permeable to cations
  • found on the post junctional muscle membrane of skeletal muscle
31
Q

Outline the process of how the skeletal muscle become depolarised

A
  1. ACh binds to nAChR on the skeletal muscle memb
  2. This binding causes the ligand gated channel to open and become permeable to Na+and K+
  3. Na+ moves in to the skeletal muscle causing depolarisation known as an end-plate potential
  4. This depolarisation raises the adjacent membrane potential above threshold so that an AP is initiated in the skeletal muscle –> contraction
32
Q

What is the name of the potential that initiates a muscle action potential?

A

End plate potential

33
Q

a) What are neuromuscular blocks?
b) Types
c) what are they used for?

A

a) Pharmaceutical agents that block nACh receptors
b)
1. COMPETETIVE BLOCKERS e.g. tubocurarine
- compete with ACh for receptor sites
- bind to ACh receptor sites and hence block the effects of ACh and hence prevents depolarisation
- CAN BE OVERCOME IF ACH CONC INCREASED

  1. DEPOLARISING BLOCKER e.g. succinylcholine
    - mimics ACh
    - binds to nACH receptor and causes depolarisation of the membrane at motor end plate causing skeletal muscle fasciculations
    - ACh esterase cannot break it down and hence there is persistent depolarisation of motor end plate (adjacent na+ channels inactivate)
    - motor end plate becomes unresponsive due to subsequent nerve impulses (depolarised block leads to flaccid paralysis of skeletal muscle)
    - lasts 5-10 mins until other enzymes break it down

c) Neuromuscular blocking agents are used in combination of general anaesthetic to cause temporary paralysis during surgery to make the muscles more relaxed and prevent movement to make surgery easier

34
Q

What are cholinesterase inhibitors and what are they used for?

A
  • inhibit the enzyme ACh esterase (breaks down ACh in synapse)
  • increase the activity of ACh by delaying its degredation
  • administered in low doses to reverse the effects of muscle relaxants ,to treat myasthenia gravis, and to treat symptoms of Alzheimer’s disease
35
Q

a) What is Mayasthenia gravis?
b) symptoms
c) cause
d) How is is diagnosed?

A

a) autoimmune disease targetting nACh receptors
b) Profound weakness that increases with exercise

c)
- Antibodies directed against nACHR on the postsynaptic membrane of skeletal muscle cells
- Antibodies lead to loss of functional receptors by complement mediated lysis and receptor degradation
- ACh cannot bind to receptors
- end plate potentials are reduced in amplitude leading to muscle weakness and fatigue

d)
Edrophonium test
- muscle weakness is provoked
- injection of a medicine called edrophonium chloride (anticholinesterase)
- if muscle weakness relieved rapidly but temporarily then you have this
- always have resuscitation facilities

36
Q

What is the consequence of taking organophosphate poisons such as parathion and sarin?

A
  • the are ACH esterase inhibitors that form a stable irreversible covalent bond to the enzyme
  • cause paralysis
  • recovery may take weeks as synthesis of new enzymes is neededa
37
Q

If the Na+/ K+ pump were to be blocked, what would be the consequence for nerve conduction of a single action potential in a nerve fibre?

A

No consequence- ion concentration is such a minor change

38
Q

If the Na+/ K+ pump were to be blocked, what would be the consequence for nerve conduction of a train of 1000 action potentials?

A

There will be nothing to return it to normal, very high intracellular ion
e.g. No sodium gradient thus an action potential cannot be generated

Na+K+ATPase is not required for action potential re- setting mechanism
However the pump is required to re- set the membrane potential when lots have been fired

ICPP (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions